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1
benign tumor of endocrine pancreas disorder 2005:2010[pubdate] *count=100
398 results
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Items 1 to 100 of about 398
1.
Leite AR, Corrêa-Giannella ML, Dagli ML, Fortes MA, Vegas VM, Giannella-Neto D:
Fibronectin and laminin induce expression of islet cell markers in hepatic oval cells in culture.
Cell Tissue Res
; 2007 Mar;327(3):529-37
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Since no previous studies have investigated the effect of ECM proteins on the expression of islet cell markers by cultured OC, the purpose of the present study was to evaluate whether FN and LAM modulate the expression of genes related to the
endocrine pancreas
in these liver cells.
MedlinePlus Health Information.
consumer health - Stem Cells
.
Hazardous Substances Data Bank.
ALLYL ALCOHOL
.
Hazardous Substances Data Bank.
2-ACETYLAMINOFLUORENE
.
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GLUCAGON
.
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(PMID = 17149594.001).
[ISSN]
0302-766X
[Journal-full-title]
Cell and tissue research
[ISO-abbreviation]
Cell Tissue Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Biomarkers; 0 / Eye Proteins; 0 / Fibronectins; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Laminin; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Pancreatic Hormones; 0 / Propanols; 0 / Repressor Proteins; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 3W678R12M0 / allyl alcohol; 9007-92-5 / Glucagon; 9M98QLJ2DL / 2-Acetylaminofluorene
2.
Xiao X, Heimberg H:
Retraction. Adult stem cells regenerate the endocrine pancreas and normalize hyperglycaemia and insulin production in diabetic mice. Verh Dtsch Ges Pathol (2005) 89: 184-190.
Pathologe
; 2008 Nov;29 Suppl 2:289
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[Title]
Retraction. Adult stem cells regenerate the
endocrine pancreas
and normalize hyperglycaemia and insulin production in diabetic mice. Verh Dtsch Ges Pathol (2005) 89: 184-190.
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[RetractionOf]
Huss R, Xiangwei X, Heimberg H. Verh Dtsch Ges Pathol. 2005;89:184-90
[
18035689.001
]
(PMID = 19039619.001).
[ISSN]
1432-1963
[Journal-full-title]
Der Pathologe
[ISO-abbreviation]
Pathologe
[Language]
eng; ger
[Publication-type]
Retraction of Publication
[Publication-country]
Germany
3.
Gasco V, Beccuti G, Marotta F, Benso A, Granata R, Broglio F, Ghigo E:
Endocrine and metabolic actions of ghrelin.
Endocr Dev
; 2010;17:86-95
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[Title]
Endocrine
and metabolic actions of ghrelin.
This peptide, whose acylation is performed by a specific octanoyl-transferase, is predominantly produced by the stomach, although expressed by many other
endocrine
and nonendocrine, peripheral and central tissues.
GRLN receptors have been well demonstrated either in the
endocrine pancreas
or the adipose tissue; at these levels there are receptors that bind GRLN independently of its acylation (therefore a non-GHS-R1a, still undefined receptor).
[MeSH-major]
Endocrine
Glands / physiology. Ghrelin / physiology. Metabolism / physiology
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.
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Corticotropin
.
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[Copyright]
Copyright 2010 S. Karger AG, Basel.
(PMID = 19955759.001).
[ISSN]
1662-2979
[Journal-full-title]
Endocrine development
[ISO-abbreviation]
Endocr Dev
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Ghrelin; 0 / Gonadotropins; 0 / Insulin; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; IY9XDZ35W2 / Glucose
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4.
Loffler KA, Biondi CA, Gartside M, Waring P, Stark M, Serewko-Auret MM, Muller HK, Hayward NK, Kay GF:
Broad tumor spectrum in a mouse model of multiple endocrine neoplasia type 1.
Int J Cancer
; 2007 Jan 15;120(2):259-67
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[Title]
Broad
tumor
spectrum in a mouse model of multiple
endocrine
neoplasia
type 1.
Multiple
endocrine
neoplasia
type 1 (MEN1) is an inherited cancer predisposition syndrome typified by development of tumors in parathyroid, pituitary and
endocrine pancreas
, as well as less common sites including both
endocrine
and nonendocrine organs.
Deletion or mutation of the
tumor
suppressor gene MEN1 on chromosome 11 has been identified in many cases of MEN1 as well as in sporadic tumors.
Here we describe a mouse model of MEN1 in which tumors were seen in pancreatic
islets
, pituitary, thyroid and parathyroid, adrenal glands, testes and ovaries.
The observed
tumor
spectrum therefore includes types commonly seen in MEN1 patients and additional types.
Pancreatic pathology was most common, evident in over 80% of animals, while other
tumor
types developed with lower frequency and generally later onset.
Tumors of multiple
endocrine
organs were observed frequently, but progression to carcinoma and metastasis were not evident.
Menin expression was below the level of detection in ovary, thyroid and testis, but loss of nuclear menin immunoreactivity was observed uniformly in all pancreatic islet adenomas and in some hyperplastic islet cells, suggesting that complete loss of Men1 is a critical point in islet
tumor
progression in this model.
[MeSH-major]
Adenoma / pathology. Disease Models, Animal.
Endocrine
Gland Neoplasms / pathology. Mice / genetics. Multiple
Endocrine
Neoplasia
Type 1 / pathology. Proto-Oncogene Proteins / genetics
[MeSH-minor]
Animals. DNA,
Neoplasm
/ analysis. Exons / genetics. Female. Genes,
Tumor
Suppressor. Male. Peptide Chain Initiation, Translational / genetics
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Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
Marmoset Gene list: Data: Gene Annotation
.
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[Copyright]
(c) 2006 Wiley-Liss, Inc.
(PMID = 17044021.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Neoplasm; 0 / Men1 protein, mouse; 0 / Proto-Oncogene Proteins
5.
Kloosterman WP, Lagendijk AK, Ketting RF, Moulton JD, Plasterk RH:
Targeted inhibition of miRNA maturation with morpholinos reveals a role for miR-375 in pancreatic islet development.
PLoS Biol
; 2007 Aug;5(8):e203
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The aberrant formation of the
endocrine pancreas
, caused by miR-375 knockdown, is one of the first loss-of-function phenotypes for an individual miRNA in vertebrate development.
[MeSH-minor]
Animals. Base Sequence. Cell Movement / physiology. Genes, Reporter. Humans. In Situ Hybridization.
Islets
of
Langerhans
/ cytology.
Islets
of
Langerhans
/ embryology.
Islets
of
Langerhans
/ metabolism. Molecular Sequence Data. Phenotype. RNA Precursors / genetics. RNA Precursors / metabolism. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Sequence Alignment. Zebrafish Proteins / genetics. Zebrafish Proteins / metabolism
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
SciCrunch.
ZFIN: Data: Gene Expression
.
The Lens.
Cited by Patents in
.
ZFIN.
ZFIN
.
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[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs; 0 / Oligonucleotides, Antisense; 0 / RNA Precursors; 0 / Recombinant Fusion Proteins; 0 / Zebrafish Proteins
[Other-IDs]
NLM/ PMC1925136
6.
Koceïr EA, Benbaïbeche H, Haffaf el M, Kacimi G, Oudjit B:
[Metabolic syndrome and hormonal interaction in obese and type 2 diabetic Algerian subject: the behavior eating disorder impact].
Ann Biol Clin (Paris)
; 2009 May-Jun;67(3):315-23
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[Title]
[Metabolic syndrome and hormonal interaction in obese and type 2 diabetic Algerian subject: the behavior eating
disorder
impact].
[Transliterated title]
Syndrome métabolique et interaction hormonale chez le sujet obèse et le patient diabétique
de
type 2 algérien: impact
des
troubles du comportement alimentaire.
In response to nutritional stress, the BED generates a hyperactivity
of endocrine pancreas
, adrenal gland, and pituitary gland.
MedlinePlus Health Information.
consumer health - Diabetes Type 2
.
MedlinePlus Health Information.
consumer health - Eating Disorders
.
MedlinePlus Health Information.
consumer health - Metabolic Syndrome
.
MedlinePlus Health Information.
consumer health - Obesity
.
Hazardous Substances Data Bank.
CHOLESTEROL
.
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(PMID = 19411234.001).
[ISSN]
0003-3898
[Journal-full-title]
Annales de biologie clinique
[ISO-abbreviation]
Ann. Biol. Clin. (Paris)
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Blood Glucose; 0 / Peptides; 0 / Triglycerides; 0 / polypeptide C; 12629-01-5 / Human Growth Hormone; 4429-04-3 / Fructosamine; 97C5T2UQ7J / Cholesterol
7.
Chan CB, Harper ME:
Uncoupling proteins: role in insulin resistance and insulin insufficiency.
Curr Diabetes Rev
; 2006 Aug;2(3):271-83
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UCP2 mRNA is expressed in a wide range of tissues; however UCP2 protein expression is restricted to fewer tissues, including the
endocrine pancreas
, spleen, stomach, brain and the lung.
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(PMID = 18220632.001).
[ISSN]
1573-3998
[Journal-full-title]
Current diabetes reviews
[ISO-abbreviation]
Curr Diabetes Rev
[Language]
ENG
[Grant]
None / None / / 43987; Canada / Canadian Institutes of Health Research / / 43987
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United Arab Emirates
[Chemical-registry-number]
0 / Insulin; 0 / Ion Channels; 0 / Mitochondrial Proteins; 0 / mitochondrial uncoupling protein 2; 0 / mitochondrial uncoupling protein 3
[Number-of-references]
168
[Other-IDs]
NLM/ CAMS820; NLM/ PMC3060851
8.
Pissios P, Ozcan U, Kokkotou E, Okada T, Liew CW, Liu S, Peters JN, Dahlgren G, Karamchandani J, Kudva YC, Kurpad AJ, Kennedy RT, Maratos-Flier E, Kulkarni RN:
Melanin concentrating hormone is a novel regulator of islet function and growth.
Diabetes
; 2007 Feb;56(2):311-9
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In this study, we further explored the role of MCH in the
endocrine pancreas
.
Both MCH and MCHR1 are expressed in mouse and human
islets
and in clonal beta-cell lines as assessed using quantitative real-time PCR and immunohistochemistry.
Interestingly, MCH enhanced insulin secretion in human and mouse
islets
and rodent beta-cell lines in a dose-dependent manner.
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gene/protein/disease-specific - Melanin-concentrating hormone receptors - overview and references
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gene/protein/disease-specific - MCH1 receptor - data and references
.
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CALCIUM, ELEMENTAL
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.
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(PMID = 17259374.001).
[ISSN]
0012-1797
[Journal-full-title]
Diabetes
[ISO-abbreviation]
Diabetes
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / K08 DK 02885; United States / NIDDK NIH HHS / DK / P30 DK040561; United States / NIDDK NIH HHS / DK / R01 DK 67536; None / None / / P30 DK040561-11; United States / NIDDK NIH HHS / DK / R01 DK 46960; United States / NIDDK NIH HHS / DK / R03 DK 66207; United States / NIDDK NIH HHS / DK / P30 DK 040561; United States / NIDDK NIH HHS / DK / P30 DK040561-11; United States / NIDDK NIH HHS / DK / R01 DK 68721; United States / NIDDK NIH HHS / DK / P01 DK 53115; United States / PHS HHS / / 5P30 36836
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Dietary Fats; 0 / Hypothalamic Hormones; 0 / Insulin; 0 / Melanins; 0 / Pituitary Hormones; 0 / Receptors, Pituitary Hormone; 0 / melanin-concentrating hormone receptor; 67382-96-1 / melanin-concentrating hormone; SY7Q814VUP / Calcium
9.
Gesase AP, Satoh Y:
Morphology of neuropeptide Y immunopositive ganglia in the mouse pancreas.
Ital J Anat Embryol
; 2006 Jul-Sep;111(3):171-8
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[Title]
Morphology of neuropeptide Y immunopositive ganglia in the mouse
pancreas
.
The current immunohistochemical study used the antibody against neuropeptide Y (NPY) to observe the morphology of the autonomic ganglia in the mouse
pancreas
.
Two types of ganglia were observed and they included the
endocrine
-contact ganglia that made contact with the
endocrine pancreas
and the interstitial ganglia, which were located in the interstitial space.
The interstitial ganglia showed intense NPY-immunostaining than the
endocrine
-contact ganglia and were also closely associated with the NPY-immunopositive nerve fibres and varicose nerve fibres compared to the
endocrine
-contact ganglia.
The
endocrine
-contact ganglia were also stained positively against the NPY, but the intensity of staining was weaker compared to that of the interstitial ganglia.
The ganglia were seen to have a direct contact with NPY-immunopositive cells of the
endocrine pancreas
.
Endocrine
-contact ganglia were associated with a few NPY-immunopostive varicose nerve fibres but were not in contact with NPY-immunopoisitive large nerve bundles.
The current observation revealed that the interstitial ganglia of the mouse
pancreas
showed intense NPY-immunoreactivity compared to
endocrine
contact ganglia and that the interstitial ganglia are associated with numerous NPY-immunopositive nerve terminals.
[MeSH-major]
Ganglia, Autonomic / metabolism. Neurons / metabolism. Neuropeptide Y / metabolism.
Pancreas
/ innervation
[MeSH-minor]
Animals. Autonomic Pathways / cytology. Autonomic Pathways / metabolism. Blood Vessels / cytology. Blood Vessels / innervation. Blood Vessels / metabolism. Cell Shape / physiology. Immunohistochemistry.
Islets
of
Langerhans
/ cytology.
Islets
of
Langerhans
/ innervation.
Islets
of
Langerhans
/ metabolism. Male. Mice. Mice, Inbred BALB C. Microcirculation / cytology. Microcirculation / innervation. Microcirculation / metabolism. Presynaptic Terminals / metabolism. Presynaptic Terminals / ultrastructure
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(PMID = 17312923.001).
[ISSN]
1122-6714
[Journal-full-title]
Italian journal of anatomy and embryology = Archivio italiano di anatomia ed embriologia
[ISO-abbreviation]
Ital J Anat Embryol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Neuropeptide Y
10.
Gustavsen CR, Pillay N, Heller RS:
An immunohistochemical study of the endocrine pancreas of the African ice rat, Otomys sloggetti robertsi.
Acta Histochem
; 2008;110(4):294-301
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[Title]
An immunohistochemical study of the
endocrine pancreas
of the African ice rat, Otomys sloggetti robertsi.
The study reported here examines the
endocrine pancreas
of this species using immunohistochemical techniques.
The
islets
of
Langerhans
were scattered in the exocrine
pancreas
and tended to be quite small.
Scattered single
endocrine
cells (mostly immunoreactive for insulin) were found in the exocrine
pancreas
and were not generally associated with ducts (as marked by pan-cytokeratin labeling).
The normal islet architecture of insulin in the center and glucagon, somatostatin (SS) and pancreatic polypeptide (PP) in the rim was observed, but the
islets
tended to have 2-3 layers of glucagon immunoreactive cells.
Examining for rarer
endocrine
cell types, we found that cocaine amphetamine regulated transcript (CART) immunoreactive cells were co-localized with SS; and peptide YY (PYY) immunoreactive cells could be found that were singly immunoreactive or co-localized with either PP or glucagon.
The Nkx family of transcription factors (Nkx6.1 and 2.2) and PDX-1 were all detected in the
pancreas
in a similar manner to that seen in mouse and rat.
In conclusion, the
endocrine pancreas
of the African ice rat is quite similar to that of other studied rodents, but these animals have more glucagon and SS cells than rat (Rattus) or mouse (Mus) species.
[MeSH-major]
Islets
of
Langerhans
/ metabolism. Murinae / metabolism
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(PMID = 18406449.001).
[ISSN]
0065-1281
[Journal-full-title]
Acta histochemica
[ISO-abbreviation]
Acta Histochem.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Hormones; 0 / Transcription Factors
11.
Foo KS, Brauner H, Ostenson CG, Broberger C:
Nucleobindin-2/nesfatin in the endocrine pancreas: distribution and relationship to glycaemic state.
J Endocrinol
; 2010 Mar;204(3):255-63
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[Title]
Nucleobindin-2/nesfatin in the
endocrine pancreas
: distribution and relationship to glycaemic state.
Given the overlap of signalling molecules between the brain and
pancreas
, we have explored the presence of NUCB2 in the
islets
of
Langerhans
.
NUCB2-like immunoreactivity was detected by immunofluorescence in all human and rat islet beta-cells (as detected by co-localization with insulin), but not in other islet cells or in the exocrine
pancreas
.
Islet NUCB2 content, as measured by enzyme immunoassay, did not change significantly following an overnight fast, but was substantially lower in
islets
isolated from an animal model of type 2 diabetes, the Goto-Kakizaki (GK) rats (48% of non-diabetic Wistar rat control).
The release of NUCB2 from isolated rat
islets
was significantly elevated following glucose challenge (123%), but this effect was substantially lower than that observed for insulin (816%).
However, our findings, together with previous reports, appear more compatible with intracellular actions rather than with
endocrine
/paracrine communication, and suggest that NUCB2 in serum derives primarily from non-islet sources.
[MeSH-major]
Calcium-Binding Proteins / metabolism. DNA-Binding Proteins / metabolism. Glucose / metabolism.
Islets
of
Langerhans
/ metabolism
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
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(PMID = 20032201.001).
[ISSN]
1479-6805
[Journal-full-title]
The Journal of endocrinology
[ISO-abbreviation]
J. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Calcium-Binding Proteins; 0 / DNA-Binding Proteins; 0 / Nerve Tissue Proteins; 0 / nucleobindin; IY9XDZ35W2 / Glucose
12.
Somm E, Schwitzgebel VM, Vauthay DM, Camm EJ, Chen CY, Giacobino JP, Sizonenko SV, Aubert ML, Hüppi PS:
Prenatal nicotine exposure alters early pancreatic islet and adipose tissue development with consequences on the control of body weight and glucose metabolism later in life.
Endocrinology
; 2008 Dec;149(12):6289-99
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In the present study, we investigated the impact of prenatal nicotine exposure (3 mg/kg in Sprague Dawley rats via osmotic Alzet minipumps) on the early
endocrine pancreas
and adipose tissue development in rat pups before weaning.
Prenatal nicotine exposure led to a decrease in
endocrine
pancreatic islet size and number at 7 d of life (postnatal d 7), which corroborates with a decrease in gene expression of specific transcription factors such as pancreatic and duodenal homeobox 1, Pax-6, Nkx6.1, and of hormones such as insulin and glucagon.
[MeSH-major]
Body Weight / drug effects. Glucose / metabolism.
Islets
of
Langerhans
/ drug effects. Nicotine / toxicity. Prenatal Exposure Delayed Effects / metabolism
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(PMID = 18687784.001).
[ISSN]
0013-7227
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Ganglionic Stimulants; 6M3C89ZY6R / Nicotine; IY9XDZ35W2 / Glucose
13.
Pasquali L, Fan Y, Trucco M, Ringquist S:
Rehabilitation of adaptive immunity and regeneration of beta cells.
Trends Biotechnol
; 2006 Nov;24(11):516-22
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Recent observations illustrating the regenerative capability of the
endocrine pancreas
in addition to advances in stem cell and gene therapy technologies enable the exploration of alternatives to allogeneic islet transplantation.
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(PMID = 16963140.001).
[ISSN]
0167-7799
[Journal-full-title]
Trends in biotechnology
[ISO-abbreviation]
Trends Biotechnol.
[Language]
eng
[Grant]
United States / NIAID NIH HHS / AI / U19 AI 056374-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
[Publication-country]
England
[Chemical-registry-number]
0 / HLA-DQ Antigens
[Number-of-references]
86
14.
Chianelli M, Parisella MG, Visalli N, Mather SJ, D'Alessandria C, Pozzilli P, Signore A, IMDIAB study group:
Pancreatic scintigraphy with 99mTc-interleukin-2 at diagnosis of type 1 diabetes and after 1 year of nicotinamide therapy.
Diabetes Metab Res Rev
; 2008 Feb;24(2):115-22
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[Title]
Pancreatic scintigraphy with 99mTc-interleukin-2 at
diagnosis
of type 1 diabetes and after 1 year of nicotinamide therapy.
BACKGROUND: To evaluate the clinical utility of pancreatic scintigraphy with 99mTc-interleukin-2 to identify Type 1 diabetic patients with pancreatic inflammation at
diagnosis
.
RESULTS: Significant pancreatic accumulation of 99mTc-interleukin-2 was found in 31% of the patients at the time of
diagnosis
.
Patients positive or negative for pancreatic accumulation of interleukin-2 scintigraphy did not show any difference in metabolic or immunologic parameters at
diagnosis
.
Positive patients, however, showed higher C-peptide values at 3 months and lower insulin requirement at 1 year, compared to negative patients (insulin requirement (IR): 0.33+/-0.11 vs 0.67+/-0.24 IU/kg/day, positive vs negative patients; p=0.0001); patients positive to IL2 scintigraphy treated with nicotinamide at 25 mg/kg were the only group showing a significant reduction in IR 1 year after
diagnosis
(IRt0: 0.53+/-0.30 vs IRt12: 0.28+/-0.07 IU/kg/day; p=0.013).
After 1 year, all the positive patients showed a significant decrease in pancreatic uptake of 99mTc-interleukin-2 (P/B: 7.87+/-2.28 at
diagnosis
vs 5.00+/-1.23 after 1 year; p<0.0001 paired t-test).
CONCLUSION: 99mTc-interleukin-2 scintigraphy at
diagnosis
of Type 1 diabetes may identify patients with pancreatic inflammation.
In such patients, treated with nicotinamide at 25 mg/kg, insulin requirement and pancreatic inflammation after 1 year were significantly reduced suggesting that IL2 scintigraphy may be of potential use for assessing the autoimmune phenomena in
endocrine pancreas
.
[MeSH-major]
Diabetes Mellitus, Type 1 / drug therapy. Diabetes Mellitus, Type 1 / radionuclide imaging. Interleukin-2. Niacinamide / therapeutic use. Organotechnetium Compounds.
Pancreas
/ radionuclide imaging
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[Copyright]
Copyright (c) 2007 John Wiley & Sons, Ltd.
(PMID = 17918277.001).
[ISSN]
1520-7552
[Journal-full-title]
Diabetes/metabolism research and reviews
[ISO-abbreviation]
Diabetes Metab. Res. Rev.
[Language]
eng
[Publication-type]
Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Interleukin-2; 0 / Organotechnetium Compounds; 0 / technetium Tc 99m interleukin 2; 25X51I8RD4 / Niacinamide
15.
Krishnamurthy M, Wang R:
Integrins and extracellular matrices in pancreatic tissue engineering.
Front Biosci (Schol Ed)
; 2009;1:477-91
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The role of integrin receptors in regulating numerous cellular programs have been well studied in the
endocrine pancreas
.
These adhesion receptors and their interactions with the extracellular matrix (ECM) are important determinants of islet cell biology as they influence the development, survival and function of the
islets
of
Langerhans
.
[MeSH-major]
Extracellular Matrix / physiology. Integrins / physiology.
Islets
of
Langerhans
/ cytology. Tissue Engineering
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(PMID = 19482715.001).
[ISSN]
1945-0524
[Journal-full-title]
Frontiers in bioscience (Scholar edition)
[ISO-abbreviation]
Front Biosci (Schol Ed)
[Language]
eng
[Grant]
Canada / Canadian Institutes of Health Research / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Integrins
[Number-of-references]
115
16.
Beatriz Di Carlo M, López Mingorance FN, del Carmen Maselli M, Hamamura S, Otero G, Tiscornia OM, Negri GA:
[Biochemical profile of the pancreatic function: pancreolauril and oral glucose tolerance tests].
Acta Gastroenterol Latinoam
; 2010 Jun;40(2):128-33
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[Transliterated title]
Evaluación bioquímica
de
la función pancreática: Pruebas del pancreolauril y
de
la tolerancia a la glucosa oral.
BACKGROUND: The
pancreas
is a mixed gland that takes part in the digestion of nutrients and in the homeostasis ofglycemia.
Chronic pancreopathy is the cause of secretory insufficiency, characterized by an inflammatory process that leads to fibrosis of the
pancreas
, with a progressive loss of both exocrine and
endocrine
functions of the gland.
OBJECTIVE: To study both the exocrine and
endocrine
pancreatic relationship in patients with pancreatopathies and other non-pancreatic digestive alterations, by means of serum pancreolauril (sPL) and oral glucose tolerance tests (OGTT).
From the latter group, a subgroup (n=11) with a
diagnosis
of chronic pancreatitis (CP) was studied.
CONCLUSION: By the biochemical tests used,
pancreas
functionality corresponds with a close relationship between exocrine and
endocrine pancreas
.
Thus, we suggest the use of the sPL test as a helpful tool for the
diagnosis
of CP.
[MeSH-major]
Fluoresceins. Glucose / analysis. Glucose Tolerance Test.
Pancreas
, Exocrine / physiopathology. Pancreatitis, Chronic / blood
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(PMID = 20645560.001).
[ISSN]
0300-9033
[Journal-full-title]
Acta gastroenterologica Latinoamericana
[ISO-abbreviation]
Acta Gastroenterol. Latinoam.
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Argentina
[Chemical-registry-number]
0 / Fluoresceins; 939U41013O / fluorescein dilaurate; EC 3.1.1.3 / Lipase; EC 3.2.1.- / Amylases; IY9XDZ35W2 / Glucose
17.
Fowden AL, Giussani DA, Forhead AJ:
Endocrine and metabolic programming during intrauterine development.
Early Hum Dev
; 2005 Sep;81(9):723-34
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[Title]
Endocrine
and metabolic programming during intrauterine development.
Many of these metabolic disorders have an
endocrine
origin and are accompanied by abnormal hormone concentrations.
This has led to the hypothesis that adult metabolic disease arises in utero as a result of programming of key
endocrine
systems during suboptimal intrauterine conditions associated with fetal growth retardation.
This review examines the experimental evidence for prenatal
endocrine
programming with particular emphasis on
endocrine
axes involved in growth and metabolism, namely, the hypothalamic-pituitary-adrenal axis, the
endocrine pancreas
and the somatotrophic axis.
It also considers how changes in these
endocrine
systems contribute to the programming of metabolism in later life.
[MeSH-major]
Endocrine
System / embryology. Fetal Development. Metabolism
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(PMID = 16085373.001).
[ISSN]
0378-3782
[Journal-full-title]
Early human development
[ISO-abbreviation]
Early Hum. Dev.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Hormones
[Number-of-references]
29
18.
Noone TC, Hosey J, Firat Z, Semelka RC:
Imaging and localization of islet-cell tumours of the pancreas on CT and MRI.
Best Pract Res Clin Endocrinol Metab
; 2005 Jun;19(2):195-211
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[Title]
Imaging and localization of islet-cell tumours of the
pancreas
on CT and MRI.
Islet-cell tumours are neuroendocrine tumours that arise from the
endocrine pancreas
.
They range from
benign
to malignant.
[MeSH-major]
Adenoma, Islet Cell /
diagnosis
. Magnetic Resonance Imaging / methods. Pancreatic Neoplasms /
diagnosis
. Tomography, X-Ray Computed / methods
[MeSH-minor]
Gastrinoma /
diagnosis
. Humans. Insulinoma /
diagnosis
.
Islets
of
Langerhans
/ pathology. Multiple
Endocrine
Neoplasia
Type 1 /
diagnosis
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(PMID = 15763695.001).
[ISSN]
1521-690X
[Journal-full-title]
Best practice & research. Clinical endocrinology & metabolism
[ISO-abbreviation]
Best Pract. Res. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Review
[Publication-country]
England
[Number-of-references]
19
19.
Stosic-Grujicic S, Stojanovic I, Maksimovic-Ivanic D, Momcilovic M, Popadic D, Harhaji L, Miljkovic D, Metz C, Mangano K, Papaccio G, Al-Abed Y, Nicoletti F:
Macrophage migration inhibitory factor (MIF) is necessary for progression of autoimmune diabetes mellitus.
J Cell Physiol
; 2008 Jun;215(3):665-75
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Furthermore, MIF-deficient (MIF(-/-)) mice were less susceptible to the induction of immunoinflammatory diabetes, insulitis and apoptosis within the
endocrine pancreas
by multiple low doses of streptozotocin (MLD-STZ) than genetically matched wild type (WT) mice.
Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1beta, and iNOS in the
islets
of
Langerhans
.
These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the
pancreas of
MLD-STZ-challenged MIF(-/-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response.
[MeSH-minor]
Adoptive Transfer. Animals. Antibodies, Monoclonal / pharmacology. Cell Adhesion / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Cyclophosphamide / administration & dosage. Cyclophosphamide / pharmacology. Cytokines / biosynthesis. Cytokines / genetics. Disease Progression. Female. Gene Expression Regulation / drug effects.
Islets
of
Langerhans
/ drug effects.
Islets
of
Langerhans
/ enzymology.
Islets
of
Langerhans
/ pathology. Leukocytes, Mononuclear / drug effects. Mice. Mice, Inbred NOD. Nitric Oxide / metabolism. Nitric Oxide Synthase Type II / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. Spleen / drug effects. Spleen / pathology. Streptozocin. Tyrosine / analogs & derivatives. Tyrosine / metabolism
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[Copyright]
(c) 2007 Wiley-Liss, Inc.
(PMID = 18064633.001).
[ISSN]
1097-4652
[Journal-full-title]
Journal of cellular physiology
[ISO-abbreviation]
J. Cell. Physiol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibodies, Monoclonal; 0 / Cytokines; 0 / Macrophage Migration-Inhibitory Factors; 0 / RNA, Messenger; 31C4KY9ESH / Nitric Oxide; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 5W494URQ81 / Streptozocin; 8N3DW7272P / Cyclophosphamide; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.2.1 / Mif protein, mouse
20.
Bolkent S, Bolkent S, Yanardag R, Tunali S:
Protective effect of vanadyl sulfate on the pancreas of streptozotocin-induced diabetic rats.
Diabetes Res Clin Pract
; 2005 Nov;70(2):103-9
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[Title]
Protective effect of vanadyl sulfate on the
pancreas of
streptozotocin-induced diabetic rats.
The aim of this study is to examine from a biochemical and histological perspective, whether vanadium has a protective effect on the
pancreas of
diabetic rats.
On day 60, the
pancreas
tissue and blood samples were taken from the animals.
In pancreatic
islets
of the diabetic group, a decrease in the number of immunoreactive B cells was observed in comparison to the control group.
On the other hand, pancreatic
islets
of the diabetic group given vanadyl sulfate showed a higher number of immunoreactive B cells in comparison to the diabetic group.
According to the immunohistochemical and biochemical results obtained, it was concluded that vanadyl sulfate can regenerate B cells
of endocrine pancreas
in experimental diabetes.
[MeSH-major]
Diabetes Mellitus, Experimental / drug therapy. Hypoglycemic Agents / pharmacology.
Pancreas
/ drug effects. Vanadium Compounds / pharmacology. Vanadium Compounds / therapeutic use
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.
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(PMID = 16188572.001).
[ISSN]
0168-8227
[Journal-full-title]
Diabetes research and clinical practice
[ISO-abbreviation]
Diabetes Res. Clin. Pract.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Blood Glucose; 0 / Hypoglycemic Agents; 0 / Vanadium Compounds; 6DU9Y533FA / vanadyl sulfate
21.
Drucker DJ:
The role of gut hormones in glucose homeostasis.
J Clin Invest
; 2007 Jan;117(1):24-32
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Among the specialized cell types in the gastrointestinal mucosa, enteroendocrine cells have important roles in regulating energy intake and glucose homeostasis through their actions on peripheral target organs, including the
endocrine pancreas
.
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(PMID = 17200703.001).
[ISSN]
0021-9738
[Journal-full-title]
The Journal of clinical investigation
[ISO-abbreviation]
J. Clin. Invest.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Glycoproteins; 0 / Insulin; 55963-74-1 / Proglucagon; 9007-92-5 / Glucagon; EC 3.4.14.5 / DPP4 protein, human; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.5.4.4 / Adenosine Deaminase
[Number-of-references]
125
[Other-IDs]
NLM/ PMC1716213
22.
Strowski MZ, Kaczmarek P, Mergler S, Wiedenmann B, Domin D, Szwajkowski P, Wojciechowicz T, Skrzypski M, Szczepankiewicz D, Szkudelski T, Rucinski M, Malendowicz LK, Nowak KW:
Insulinostatic activity of cerebellin--evidence from in vivo and in vitro studies in rats.
Regul Pept
; 2009 Oct 9;157(1-3):19-24
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Cbln is also expressed in the
pancreas
; however, its function in the
pancreas
is unknown.
We identified Cbln1 and Cbln3 transcripts in rat pancreatic
islets
and detected Cbln-immunoreactivity, predominantly located in the periphery of the rat
endocrine pancreas
.
CER decreased insulin secretion from isolated rat pancreatic
islets
at high (11 mM), but not at low (3.33 mM) glucose concentration.
Our study demonstrates for the first time that Cbln1 and Cbln3 are expressed in the rat
endocrine pancreas
.
[MeSH-minor]
Animals. Calcium / analysis. Cell Line. Cyclic AMP / analysis. Female.
Islets
of
Langerhans
/ drug effects.
Islets
of
Langerhans
/ metabolism.
Islets
of
Langerhans
/ secretion.
Pancreas
, Exocrine / drug effects.
Pancreas
, Exocrine / metabolism.
Pancreas
, Exocrine / secretion. Protein Precursors / genetics. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction
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CALCIUM, ELEMENTAL
.
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(PMID = 19481574.001).
[ISSN]
1873-1686
[Journal-full-title]
Regulatory peptides
[ISO-abbreviation]
Regul. Pept.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Insulin; 0 / Nerve Tissue Proteins; 0 / Protein Precursors; 94071-26-8 / cerebellin; E0399OZS9N / Cyclic AMP; SY7Q814VUP / Calcium
23.
Umeda H, Ozaki N, Mizutani N, Fukuyama T, Nagasaki H, Arima H, Oiso Y:
Protective effect of hedgehog signaling on cytokine-induced cytotoxicity in pancreatic beta-cells.
Exp Clin Endocrinol Diabetes
; 2010 Nov;118(10):692-8
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BACKGROUND: Hedgehog (Hh) signaling plays an important role in
pancreas
development.
However, its role in the developed
endocrine pancreas
remains to be elucidated.
The Hh signal inhibitor cyclopamine were pretreated in INS-1E cells and rat
islets
.
RESULTS: We found that exposure to proinflammatory cytokines increased Ihh expression in rat
islets
and INS-1E cells.
By contrast, treatment with cyclopamine increased cytokine-induced apoptosis in INS-1E cells and rat
islets
.
[MeSH-minor]
Animals. Apoptosis / drug effects. Cell Line. Diabetes Mellitus, Type 1 / immunology. Gene Expression Regulation / drug effects. Gene Silencing.
Islets
of
Langerhans
/ drug effects.
Islets
of
Langerhans
/ metabolism.
Islets
of
Langerhans
/ pathology. Male. NF-kappa B / genetics. NF-kappa B / metabolism. Nitric Oxide Synthase Type II / metabolism. Organ Culture Techniques. RNA, Messenger / metabolism. RNA, Small Interfering. Rats. Veratrum Alkaloids / pharmacology
Hazardous Substances Data Bank.
CYCLOPAMINE
.
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[Copyright]
© J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart · New York.
(PMID = 20533175.001).
[ISSN]
1439-3646
[Journal-full-title]
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
[ISO-abbreviation]
Exp. Clin. Endocrinol. Diabetes
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Cytokines; 0 / Dhh protein, rat; 0 / Hedgehog Proteins; 0 / Ihh protein, rat; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Veratrum Alkaloids; 0 / sonic hedgehog protein, rat; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; ZH658AJ192 / cyclopamine
24.
Portha B, Lacraz G, Chavey A, Figeac F, Fradet M, Tourrel-Cuzin C, Homo-Delarche F, Giroix MH, Bailbé D, Gangnerau MN, Movassat J:
Islet structure and function in the GK rat.
Adv Exp Med Biol
; 2010;654:479-500
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Type 2 diabetes mellitus (T2D) arises when the
endocrine pancreas
fails to secrete sufficient insulin to cope with the metabolic demand because of beta-cell secretory dysfunction and/or decreased beta-cell mass.
Defining the nature of the pancreatic islet defects present in T2D has been difficult, in part because human
islets
are inaccessible for direct study.
(ii) gestational metabolic impairment inducing an epigenetic programming of the offspring
pancreas
(decreased beta-cell neogenesis and proliferation) transmitted over generations; and (iii) loss of beta-cell differentiation related to chronic exposure to hyperglycaemia/hyperlipidaemia, islet inflammation, islet oxidative stress, islet fibrosis and perturbed islet vasculature.
[MeSH-major]
Diabetes Mellitus, Type 2 / metabolism.
Islets
of
Langerhans
/ cytology
[MeSH-minor]
Animals. Cell Differentiation. Cell Survival. Disease Models, Animal.
Endocrine
System. Epigenesis, Genetic. Insulin-Secreting Cells / cytology. Mice. Models, Biological. Oxidative Stress. Rats. Reactive Oxygen Species
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(PMID = 20217511.001).
[ISSN]
0065-2598
[Journal-full-title]
Advances in experimental medicine and biology
[ISO-abbreviation]
Adv. Exp. Med. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Reactive Oxygen Species
[Number-of-references]
111
25.
Johansson T, Lejonklou MH, Ekeblad S, Stålberg P, Skogseid B:
Lack of nuclear expression of hairy and enhancer of split-1 (HES1) in pancreatic endocrine tumors.
Horm Metab Res
; 2008 May;40(5):354-9
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[Title]
Lack of nuclear expression of hairy and enhancer of split-1 (HES1) in pancreatic
endocrine
tumors.
Cell line experiments have suggested the involvement of Notch signaling in pancreatic
endocrine
tumorigenesis.
We investigated the expression of NOTCH1, HES1, HEY1 and ASCL1 in pancreatic
endocrine
tumors and compared the data to
tumor
phenotype including hormone production, heredity, and WHO classification.
Real-time quantitative PCR and immunohistochemistry were performed on samples of 26 pancreatic
endocrine
tumors.
For comparison, 10 specimens of macroscopically normal
pancreas
were analyzed using immunohistochemistry.
In the nontumorous pancreatic
endocrine
cells, weak nuclear expression of HES1 as well as of HEY1 and NOTCH1 was observed.
This lack of nuclear expression of HES1 may contribute to the abundance of ASCL1 and to tumorigenesis in the
endocrine pancreas
.
[MeSH-major]
Basic Helix-Loop-Helix Transcription Factors / biosynthesis. Cell Nucleus / metabolism. Cell Transformation, Neoplastic / metabolism. Gene Expression Regulation, Neoplastic. Homeodomain Proteins / biosynthesis.
Neoplasm
Proteins / biosynthesis. Pancreatic Neoplasms / metabolism
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(PMID = 18491256.001).
[ISSN]
0018-5043
[Journal-full-title]
Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et métabolisme
[ISO-abbreviation]
Horm. Metab. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / ASCL1 protein, human; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Cell Cycle Proteins; 0 / HEY1 protein, human; 0 / Homeodomain Proteins; 0 / NOTCH1 protein, human; 0 / Neoplasm Proteins; 0 / Receptor, Notch1; 149348-15-2 / HES1 protein, human
26.
McIntosh CH, Widenmaier S, Kim SJ:
Pleiotropic actions of the incretin hormones.
Vitam Horm
; 2010;84:21-79
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The insulin secretory response to a meal results largely from glucose stimulation of the pancreatic
islets
and both direct and indirect (autonomic) glucose-dependent stimulation by incretin hormones released from the gastrointestinal tract.
Localization of the cognate G protein-coupled receptors for GIP and GLP-1 revealed that they are present in numerous tissues in addition to the
endocrine pancreas
, including the gastrointestinal, cardiovascular, central nervous and autonomic nervous systems (ANSs), adipose tissue, and bone.
[MeSH-major]
Gastric Inhibitory Polypeptide / physiology. Glucagon-Like Peptide 1 / physiology. Insulin / physiology.
Islets
of
Langerhans
/ physiology
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
(PMID = 21094896.001).
[ISSN]
0083-6729
[Journal-full-title]
Vitamins and hormones
[ISO-abbreviation]
Vitam. Horm.
[Language]
eng
[Grant]
Canada / Canadian Institutes of Health Research / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Insulin; 0 / Receptors, Glucagon; 59392-49-3 / Gastric Inhibitory Polypeptide; 89750-14-1 / Glucagon-Like Peptide 1
27.
Boonen K, Baggerman G, D'Hertog W, Husson SJ, Overbergh L, Mathieu C, Schoofs L:
Neuropeptides of the islets of Langerhans: a peptidomics study.
Gen Comp Endocrinol
; 2007 Jun-Jul;152(2-3):231-41
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[Title]
Neuropeptides of the
islets
of
Langerhans
: a peptidomics study.
Neuropeptides from the
endocrine pancreas
(the
islets
of
Langerhans
) play an important role in the regulation of blood glucose levels.
Therefore, our aim is to identify the "peptidome" (the in vivo peptide profile at a certain time) of the pancreatic
islets
, which is beneficial for medical progress related to the treatment of diabetes.
So far, there are few neuropeptides isolated and sequenced from the
endocrine pancreas
and mainly in situ hybridisation and immunocytochemical techniques have been used to demonstrate the occurrence of peptides in the
pancreas
.
We have analysed the peptidome of the
islets
using peptidomics, i.e. a combination of liquid chromatography, mass spectrometry and bioinformatics.
We are able to identify the peptidome of
islets
extracts.
[MeSH-major]
Islets
of
Langerhans
/ metabolism. Neuropeptides / metabolism. Proteomics
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(PMID = 17559849.001).
[ISSN]
0016-6480
[Journal-full-title]
General and comparative endocrinology
[ISO-abbreviation]
Gen. Comp. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Amyloid; 0 / Blood Glucose; 0 / Chromogranin A; 0 / Chromogranin B; 0 / Islet Amyloid Polypeptide; 0 / Nerve Tissue Proteins; 0 / Neuropeptides; 0 / Pcsk1n protein, mouse; 0 / Protein Precursors; 0 / Secretogranin II; 0 / chromogranin A, mouse; 0 / chromogranin B, mouse; 0 / secretogranin 2, mouse; 106388-42-5 / Peptide YY; 51110-01-1 / Somatostatin; 55963-74-1 / Proglucagon; 74315-46-1 / prosomatostatin; 9035-68-1 / Proinsulin
28.
Otonkoski T, Näntö-Salonen K, Seppänen M, Veijola R, Huopio H, Hussain K, Tapanainen P, Eskola O, Parkkola R, Ekström K, Guiot Y, Rahier J, Laakso M, Rintala R, Nuutila P, Minn H:
Noninvasive diagnosis of focal hyperinsulinism of infancy with [18F]-DOPA positron emission tomography.
Diabetes
; 2006 Jan;55(1):13-8
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[Title]
Noninvasive
diagnosis
of focal hyperinsulinism of infancy with [18F]-DOPA positron emission tomography.
Congenital hyperinsulinism of infancy (CHI) is characterized by severe hypoglycemia due to dysregulated insulin secretion, associated with either focal or diffuse pathology of the
endocrine pancreas
.
Five patients had a visually apparent focal accumulation of [(18)F]-DOPA and standardized uptake value (SUV) >50% higher (mean 1.8-fold) than the maximum SUV of the unaffected part of the
pancreas
.
The remaining nine patients had diffuse accumulation of [(18)F]-DOPA in the
pancreas
(SUV ratio <1.5).
[MeSH-major]
Congenital Hyperinsulinism /
diagnosis
. Levodopa. Positron-Emission Tomography / methods
[MeSH-minor]
Child, Preschool. Fluorine Radioisotopes. Humans. Infant. Infant, Newborn. Mutation.
Pancreas
/ metabolism
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(PMID = 16380471.001).
[ISSN]
0012-1797
[Journal-full-title]
Diabetes
[ISO-abbreviation]
Diabetes
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Fluorine Radioisotopes; 46627O600J / Levodopa
29.
Li Z, Korzh V, Gong Z:
Localized rbp4 expression in the yolk syncytial layer plays a role in yolk cell extension and early liver development.
BMC Dev Biol
; 2007;7:117
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Since exocrine
pancreas
,
endocrine pancreas
, intestine and heart developed normally in Rbp4 morphants, we suggest that rbp4 expression in the YSL is required only for liver development.
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.
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.
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[ISSN]
1471-213X
[Journal-full-title]
BMC developmental biology
[ISO-abbreviation]
BMC Dev. Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / Rbp4 protein, zebrafish; 0 / Retinol-Binding Proteins, Plasma; 0 / Zebrafish Proteins
[Other-IDs]
NLM/ PMC2198918
30.
Rubio-Cabezas O, Minton JA, Kantor I, Williams D, Ellard S, Hattersley AT:
Homozygous mutations in NEUROD1 are responsible for a novel syndrome of permanent neonatal diabetes and neurological abnormalities.
Diabetes
; 2010 Sep;59(9):2326-31
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Studies in mice suggest that this basic helix-loop-helix transcription factor is critical in the development
of endocrine
cell lineage.
Both patients had permanent diabetes diagnosed in the first 2 months of life with no evidence of exocrine pancreatic dysfunction and a morphologically normal
pancreas
on abdominal imaging.
This syndrome highlights the critical role of NEUROD1 in both the development of the
endocrine pancreas
and the central nervous system in humans.
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.
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.
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[ISSN]
1939-327X
[Journal-full-title]
Diabetes
[ISO-abbreviation]
Diabetes
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / NEUROD1 protein, human; 9007-49-2 / DNA
[Other-IDs]
NLM/ PMC2927956
31.
Søndergaard LG, Stoltenberg M, Doering P, Flyvbjerg A, Rungby J:
Zinc ions in the endocrine and exocrine pancreas of zinc deficient rats.
Histol Histopathol
; 2006 06;21(6):619-25
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[Title]
Zinc ions in the
endocrine
and exocrine
pancreas of
zinc deficient rats.
The present study investigates how subclinical zinc deficiency in rats affects glucose metabolism and zinc distribution in the
pancreas
.
Zinc ion staining intensity of the
islets
of
Langerhans
was unaffected by the zinc deficiency.
In contrast, the acinar cells in the exocrine
pancreas
appeared depleted of iZnSAMG grains in the zinc deficient rats when compared with their controls.
Though statistically non-significant, a reduction in total zinc of the
pancreas
was found.
CONCLUSIONS: The present findings suggest that the
endocrine pancreas
is able to compensate for the subclinical zinc deficiency as it maintains an adequate zinc ion level in the secretory vesicles for insulin storage.
The exocrine
pancreas
lacks this ability; it exhibits decreased levels of zinc ion staining as a consequence of 4 weeks of reduced zinc intake.
[MeSH-major]
Islets
of
Langerhans
/ chemistry.
Pancreas
, Exocrine / chemistry. Zinc / analysis. Zinc / deficiency
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.
Hazardous Substances Data Bank.
ZINC COMPOUNDS
.
Hazardous Substances Data Bank.
ZINC SULFIDE
.
Hazardous Substances Data Bank.
GLUCOSE
.
Hazardous Substances Data Bank.
ZINC, ELEMENTAL
.
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(PMID = 16528672.001).
[ISSN]
1699-5848
[Journal-full-title]
Histology and histopathology
[ISO-abbreviation]
Histol. Histopathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Spain
[Chemical-registry-number]
0 / Blood Glucose; 0 / Insulin; 0 / Ions; 0 / Sulfides; 0 / Zinc Compounds; IY9XDZ35W2 / Glucose; J41CSQ7QDS / Zinc; KPS085631O / zinc sulfide
32.
Harries LW, Locke JM, Shields B, Hanley NA, Hanley KP, Steele A, Njølstad PR, Ellard S, Hattersley AT:
The diabetic phenotype in HNF4A mutation carriers is moderated by the expression of HNF4A isoforms from the P1 promoter during fetal development.
Diabetes
; 2008 Jun;57(6):1745-52
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RESEARCH DESIGN AND METHODS: We measured the expression of HNF4A isoforms in human adult tissues and gestationally staged fetal
pancreas
by isoform-specific real-time PCR.
The correlation between mutation position and age of
diagnosis
or age-related penetrance was assessed in a cohort of 190 patients with HNF4A mutations.
RESULTS: HNF4A was expressed exclusively from the P2 promoter in adult
pancreas
, but from 9 weeks until at least 26 weeks after conception, up to 23% of expression in fetal
pancreas
was of P1 origin.
In whole
pancreas
, HNF4A9 expression was greater than in
islets
isolated from the
endocrine pancreas
(relative level 22 vs. 7%).
CONCLUSIONS: We conclude that isoforms derived from the HNF4A P1 promoter are expressed in human fetal, but not adult,
pancreas
, and that their presence during pancreatic development may moderate the diabetic phenotype in individuals with mutations in the HNF4A gene.
[MeSH-minor]
Adult. Aged. European Continental Ancestry Group. Female. Gene Expression Profiling. Humans. Kidney / physiology. Kidney / physiopathology. Male. Middle Aged.
Pancreas
/ physiology.
Pancreas
/ physiopathology. Polymerase Chain Reaction. Protein Isoforms / genetics
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[CommentIn]
Diabetes. 2008 Jun;57(6):1461-2
[
18511449.001
]
(PMID = 18356407.001).
[ISSN]
1939-327X
[Journal-full-title]
Diabetes
[ISO-abbreviation]
Diabetes
[Language]
eng
[Grant]
United Kingdom / Wellcome Trust / / 081278/Z/06/Z
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / HNF4A protein, human; 0 / Hepatocyte Nuclear Factor 4; 0 / Protein Isoforms
33.
Dyrskog SE, Gregersen S, Hermansen K:
High-fat feeding during gestation and nursing period have differential effects on the insulin secretory capacity in offspring from normal Wistar rats.
Rev Diabet Stud
; 2005;2(3):136-45
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Restriction of protein or energy intake during gestation or early life is linked to developmental defects in the
endocrine pancreas
and insulin resistance.
After 14 wk, the
islets
of
Langerhans
were isolated for determination of insulin secretory capacity in static incubation and dynamic perifusion experiments.
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[ISSN]
1614-0575
[Journal-full-title]
The review of diabetic studies : RDS
[ISO-abbreviation]
Rev Diabet Stud
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Other-IDs]
NLM/ PMC1783557
34.
Agudo J, Ayuso E, Jimenez V, Salavert A, Casellas A, Tafuro S, Haurigot V, Ruberte J, Segovia JC, Bueren J, Bosch F:
IGF-I mediates regeneration of endocrine pancreas by increasing beta cell replication through cell cycle protein modulation in mice.
Diabetologia
; 2008 Oct;51(10):1862-72
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[Title]
IGF-I mediates regeneration
of endocrine pancreas
by increasing beta cell replication through cell cycle protein modulation in mice.
Igf1 expression in beta cells of transgenic mice regenerates the
endocrine pancreas
during type 1 diabetes.
In contrast, higher levels of cyclin-dependent kinase inhibitor 1A (p21) were detected in
islets
from non-STZ-treated transgenic mice.
Therefore, our study suggests that local production of IGF-I may be a safe approach to regenerate
endocrine pancreas
to reverse diabetes.
[MeSH-major]
Cell Cycle Proteins / metabolism. Insulin-Like Growth Factor I / metabolism. Insulin-Secreting Cells / metabolism.
Islets
of
Langerhans
/ metabolism
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[ISSN]
0012-186X
[Journal-full-title]
Diabetologia
[ISO-abbreviation]
Diabetologia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Blood Glucose; 0 / Cell Cycle Proteins; 147336-22-9 / Green Fluorescent Proteins; 5W494URQ81 / Streptozocin; 67763-96-6 / Insulin-Like Growth Factor I
35.
Behrend EN:
Update on drugs used to treat endocrine diseases in small animals.
Vet Clin North Am Small Anim Pract
; 2006 Sep;36(5):1087-105, vii
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[Title]
Update on drugs used to treat
endocrine
diseases in small animals.
Drug therapy for the
endocrine
system is implemented to replace a hormone deficiency or to prevent or reduce the formation or effects of excess hormone.
Treatment
of endocrine
disorders covers diseases of the pituitary, adrenal, parathyroid, and thyroid glands as well as the
endocrine pancreas
.
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(PMID = 16984828.001).
[ISSN]
0195-5616
[Journal-full-title]
The Veterinary clinics of North America. Small animal practice
[ISO-abbreviation]
Vet. Clin. North Am. Small Anim. Pract.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antithyroid Agents; 0 / Enzyme Inhibitors; 0 / Hypoglycemic Agents; 0 / Insulin, Long-Acting; 08J2K08A3Y / Dihydrotestosterone; 554Z48XN5E / Methimazole; L0FPV48Q5R / trilostane
[Number-of-references]
70
36.
Le D, Karmali S, Harness JK, Sheppard BC:
An update: the operative experience in adrenal, pancreatic, and other less common endocrine diseases of U.S. general surgery residents.
World J Surg
; 2008 Feb;32(2):232-6
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[Title]
An update: the operative experience in adrenal, pancreatic, and other less common
endocrine
diseases of U.S. general surgery residents.
BACKGROUND: A prior study that examined the operative experience of general surgery residents in
endocrine
surgery for the academic years 1986-1987 to 1993-1994 found this training to be inadequate due to low operative volume.
METHODS: To evaluate how the development of minimally invasive
endocrine
surgery might alter this outcome, we reviewed more recent data from the Resident Statistic Summaries (Report C) of the Residency Review Committee from 1994-1995 to 2003-2004.
For adrenalectomy, the average number of cases per resident was 1.46; for
endocrine pancreas
, the average was 0.14.
CONCLUSION: Reports from postgraduate training in laparoscopic or
endocrine
surgery suggest that these fellowships may provide the necessary additional operative experience.
[MeSH-major]
Adrenal Gland Diseases / surgery. Clinical Competence / statistics & numerical data.
Endocrine
Surgical Procedures / statistics & numerical data. General Surgery / education. Internship and Residency / statistics & numerical data. Pancreatic Diseases / surgery
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[Cites]
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8678967.001
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[
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]
(PMID = 18066698.001).
[ISSN]
0364-2313
[Journal-full-title]
World journal of surgery
[ISO-abbreviation]
World J Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
37.
Lynn FC:
Meta-regulation: microRNA regulation of glucose and lipid metabolism.
Trends Endocrinol Metab
; 2009 Nov;20(9):452-9
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MicroRNAs are key players in this regulatory milieu; they have been implicated in regulating gene expression within several metabolically active tissues including the
endocrine pancreas
, liver and adipose tissue.
[MeSH-minor]
Adipose Tissue / metabolism. Animals. Brain / metabolism. Humans.
Islets
of
Langerhans
/ metabolism. Liver / metabolism. Muscles / metabolism
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(PMID = 19800254.001).
[ISSN]
1879-3061
[Journal-full-title]
Trends in endocrinology and metabolism: TEM
[ISO-abbreviation]
Trends Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs; IY9XDZ35W2 / Glucose
[Number-of-references]
72
38.
Henopp T, Anlauf M, Schmitt A, Schlenger R, Zalatnai A, Couvelard A, Ruszniewski P, Schaps KP, Jonkers YM, Speel EJ, Pellegata NS, Heitz PU, Komminoth P, Perren A, Klöppel G:
Glucagon cell adenomatosis: a newly recognized disease of the endocrine pancreas.
J Clin Endocrinol Metab
; 2009 Jan;94(1):213-7
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[Title]
Glucagon cell adenomatosis: a newly recognized disease of the
endocrine pancreas
.
BACKGROUND: Glucagon-producing tumors are either solitary neoplasms of the
pancreas
, occasionally associated with a glucagonoma syndrome, or multiple neoplasms associated with multiple
endocrine
neoplasia
type 1 (MEN1).
We observed a previously undescribed multicentric glucagon-producing
tumor
disease that is not related to MEN1.
In addition, many
islets
were unusually large and showed glucagon cell hyperplasia.
There was no clinical or molecular evidence of any hereditary
tumor
disease, and changes in the MEN1 gene were only seen in individual tumors.
CONCLUSIONS: The findings are sufficiently distinctive to suggest a new neoplastic disease of the
endocrine pancreas
that we recommend calling glucagon cell adenomatosis.
[MeSH-minor]
Adult. Cyclin-Dependent Kinase Inhibitor p27 / genetics. Female. Humans. In Situ Hybridization, Fluorescence. Male. Proto-Oncogene Proteins / genetics. Von Hippel-Lindau
Tumor
Suppressor Protein / genetics
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(PMID = 18957496.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; 9007-92-5 / Glucagon; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
39.
Ajabnoor MA, El-Naggar MM, Elayat AA, Abdulrafee A:
Functional and morphological study of cultured pancreatic islets treated with cyclosporine.
Life Sci
; 2007 Jan 2;80(4):345-55
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[Title]
Functional and morphological study of cultured pancreatic
islets
treated with cyclosporine.
Cyclosporine A (CsA), a potent immunosuppressive drug, has been found to induce glucose intolerance through its toxic effect on the
endocrine pancreas
.
It is not exactly known whether CsA has a direct effect on the
endocrine pancreas
or induces its effect indirectly.
The present study was therefore undertaken to examine the function and morphology of isolated pancreatic
islets
when they are directly exposed in vitro to CsA.
Pancreatic
islets
were isolated from adult male Lewis rats using collagenase ductal perfusion technique.
The
islets
were separated with the discontinuous Ficoll gradient technique and further purified by hand picking of the non-islet tissue.
The
islets
were cultured in RPMI-1640, pH 7.4 and maintained at 37 degrees C in a humid atmosphere of 5% (v/v) carbon dioxide in air.
Islets
were harvested at 1, 4 and 10 days of culture and processed for functional or histological study.
The functional study of the
islets
cultured with 1 microg/ml CsA showed insulin and C-peptide contents similar to those of the control
islets
.
The
islets
cultured with 5 microg/ml CsA showed a marked decrease in insulin and C-peptide contents.
Phase contrast microscopy showed that the
islets
cultured with 1 microg/ml CsA were mostly normal looking with a well-defined regular periphery; a few
islets
had ill-defined or irregular peripheries.
The
islets
cultured with 5 microg/ml CsA had ill-defined irregular peripheries at 1 day, and were dense and forming clumps at 4 and 10 days following culture.
Islets
showed a weakly positive immunoperoxidase reaction for insulin that was weaker following the toxic dose of CsA.
It is concluded that CsA has a direct effect on B-cells that was proved by the functional and morphological changes seen in the pancreatic
islets
cultured in vitro.
[MeSH-major]
Cyclosporine / toxicity. Immunosuppressive Agents / toxicity.
Islets
of
Langerhans
/ drug effects
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(PMID = 17074365.001).
[ISSN]
0024-3205
[Journal-full-title]
Life sciences
[ISO-abbreviation]
Life Sci.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / C-Peptide; 0 / Immunosuppressive Agents; 0 / Insulin; 83HN0GTJ6D / Cyclosporine; IY9XDZ35W2 / Glucose
40.
Karaca M, Magnan C, Kargar C:
Functional pancreatic beta-cell mass: involvement in type 2 diabetes and therapeutic intervention.
Diabetes Metab
; 2009 Apr;35(2):77-84
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It is also the consequence of an inability of the
endocrine pancreas
to adapt the beta-cell mass to insulin demand (
pancreas
plasticity), which eventually leads to a decrease in functional beta-cell mass.
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(PMID = 19251449.001).
[ISSN]
1262-3636
[Journal-full-title]
Diabetes & metabolism
[ISO-abbreviation]
Diabetes Metab.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Dipeptidyl-Peptidase IV Inhibitors; 0 / Incretins; 89750-14-1 / Glucagon-Like Peptide 1; EC 3.4.14.5 / DPP4 protein, human; EC 3.4.14.5 / Dipeptidyl Peptidase 4
[Number-of-references]
52
41.
Nishi M, Sasahara M, Shono T, Saika S, Yamamoto Y, Ohkawa K, Furuta H, Nakao T, Sasaki H, Nanjo K:
A case of novel de novo paired box gene 6 (PAX6) mutation with early-onset diabetes mellitus and aniridia.
Diabet Med
; 2005 May;22(5):641-4
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[Title]
A case of novel
de
novo paired box gene 6 (PAX6) mutation with early-onset diabetes mellitus and aniridia.
PAX6 is also involved in the development of the
endocrine pancreas
, and reported to be a genetic factor common to aniridia and glucose intolerance, although the latter is usually mild.
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(PMID = 15842522.001).
[ISSN]
0742-3071
[Journal-full-title]
Diabetic medicine : a journal of the British Diabetic Association
[ISO-abbreviation]
Diabet. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / PAX6 protein; 0 / Paired Box Transcription Factors; 0 / Repressor Proteins
42.
Meivar-Levy I, Ferber S:
Regenerative medicine: using liver to generate pancreas for treating diabetes.
Isr Med Assoc J
; 2006 Jun;8(6):430-4
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[Title]
Regenerative medicine: using liver to generate
pancreas
for treating diabetes.
We review recent evidence documenting the surprising capacity of the mature liver to serve as a potential source of tissue for generating functional
endocrine pancreas
.
The process of liver-to-
pancreas
developmental redirection is induced by ectopic expression of pancreatic transcription and differentiation factors.
[MeSH-minor]
Adult. Cell Differentiation. Diabetes Mellitus, Type 2 / therapy. Humans. Immunosuppressive Agents / administration & dosage.
Islets
of
Langerhans
Transplantation. Transcription Factors / metabolism. Transcription, Genetic. Transplantation, Homologous
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(PMID = 16833177.001).
[ISSN]
1565-1088
[Journal-full-title]
The Israel Medical Association journal : IMAJ
[ISO-abbreviation]
Isr. Med. Assoc. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Israel
[Chemical-registry-number]
0 / Immunosuppressive Agents; 0 / Transcription Factors
[Number-of-references]
40
43.
Takahashi N, Kasai H:
Exocytic process analyzed with two-photon excitation imaging in endocrine pancreas.
Endocr J
; 2007 Jun;54(3):337-46
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[Title]
Exocytic process analyzed with two-photon excitation imaging in
endocrine pancreas
.
At insulin exocytosis in the pancreatic
islets
, it took two seconds for the fusion pore to dilate from 1.4 nm in diameter to 6 nm in diameter, and such unusual stability of the pore may be due to the crystallization of the intragranular contents.
[MeSH-major]
Exocytosis / physiology.
Islets
of
Langerhans
/ ultrastructure. Microscopy, Fluorescence, Multiphoton / methods. Secretory Vesicles / ultrastructure
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(PMID = 17409577.001).
[ISSN]
0918-8959
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Fluorescent Dyes; 0 / Insulin; 0 / SNARE Proteins; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
[Number-of-references]
40
44.
Koyuturk M, Ozsoy-Sacan O, Bolkent S, Yanardag R:
Effect of glurenorm on immunohistochemical changes in pancreatic beta cells of rats in experimental diabetes.
Indian J Exp Biol
; 2005 Mar;43(3):268-71
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Immunohistochemical localization of
islets
of
Langerhans
of streptozotocin (65 mg/kg, ip) induced diabetic + glurenorm (10 mg/kg, po) treated female albino rats revealed increase in number of beta cells and insulin immunoreactivity of beta cells.
The results suggest that glurenorm can cause the stimulation of beta cells
of endocrine pancreas
in diabetic rats.
[MeSH-major]
Diabetes Mellitus, Experimental / drug therapy. Hypoglycemic Agents / pharmacology. Immunohistochemistry / methods.
Islets
of
Langerhans
/ drug effects. Sulfonylurea Compounds / pharmacology
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(PMID = 15816415.001).
[ISSN]
0019-5189
[Journal-full-title]
Indian journal of experimental biology
[ISO-abbreviation]
Indian J. Exp. Biol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
India
[Chemical-registry-number]
0 / Blood Glucose; 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Sulfonylurea Compounds; C7C2QDD75P / gliquidone
45.
Youson JH, Al-Mahrouki AA, Amemiya Y, Graham LC, Montpetit CJ, Irwin DM:
The fish endocrine pancreas: review, new data, and future research directions in ontogeny and phylogeny.
Gen Comp Endocrinol
; 2006 Sep 1;148(2):105-15
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[Title]
The fish
endocrine pancreas
: review, new data, and future research directions in ontogeny and phylogeny.
The literature on the ontogeny and phylogeny of the
endocrine pancreas
of ray-finned fishes is summarized since the latest review in fish [Youson, J.H., Al-Mahrouki, A.A., 1999. Review.
Ontogenetic and phylogenetic development of the
endocrine pancreas
(islet organ) in fishes. Gen. Comp. Endocrinol.
The present study also provides the first comparative analysis of sequences of preprohormones
of endocrine
peptides from closely related basal teleost species.
[MeSH-major]
Fishes / embryology. Fishes / genetics. Fishes / physiology.
Islets
of
Langerhans
/ embryology.
Islets
of
Langerhans
/ physiology
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(PMID = 16430894.001).
[ISSN]
0016-6480
[Journal-full-title]
General and comparative endocrinology
[ISO-abbreviation]
Gen. Comp. Endocrinol.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Chemical-registry-number]
51110-01-1 / Somatostatin; 59763-91-6 / Pancreatic Polypeptide
[Number-of-references]
58
46.
Montero F, Baglietto-Vargas D, Moreno-González I, López-Tellez JF, Cuesta-Munoz AL, Gutiérrez A, Aledo JC:
Glutaminase activity is confined to the mantle of the islets of Langerhans.
Biochimie
; 2007 Nov;89(11):1366-71
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[Title]
Glutaminase activity is confined to the mantle of the
islets
of
Langerhans
.
Glutamatergic signalling plays an important role in the coordination of hormone secretion from the
endocrine pancreas
.
Recently we have reported that the
endocrine pancreas
co-expresses two isoforms of the protein glutaminase (GA), denoted as kidney-type (KGA) and liver-type (LGA).
However, how GA activity, and therefore glutamate production, is regulated in the
islets
represents a critical issue that remains unresolved.
Since the purification of these enzymes from rat
islets
is a daunting task, in order to characterize each isoform we have taken advantage of the spatial segregation of these isoenzymes in
pancreas
.
All the GA activity detected in pancreatic
islets
was attributed to KGA and was confined to the mantle of the
islets
.
Double labelling analyses strongly suggested that alpha-cells should be regarded as the site of glutamate production in the
endocrine pancreas
.
[MeSH-major]
Glutaminase / metabolism.
Islets
of
Langerhans
/ cytology.
Islets
of
Langerhans
/ enzymology
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(PMID = 17614191.001).
[ISSN]
0300-9084
[Journal-full-title]
Biochimie
[ISO-abbreviation]
Biochimie
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
France
[Chemical-registry-number]
0 / Isoenzymes; EC 3.5.1.2 / Glutaminase
47.
Eberhard D, Lammert E:
The pancreatic beta-cell in the islet and organ community.
Curr Opin Genet Dev
; 2009 Oct;19(5):469-75
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The
endocrine pancreas
consists of highly vascularized and innervated
endocrine
mini-organs--the
islets
of
Langerhans
.
Now multiple interactions with
endocrine
and nonendocrine islet cells as well as with other organs have been shown to affect the developing as well as the mature beta-cell.
[MeSH-major]
Insulin-Secreting Cells / cytology. Insulin-Secreting Cells / physiology.
Islets
of
Langerhans
.
Pancreas
The Lens.
Cited by Patents in
.
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(PMID = 19713099.001).
[ISSN]
1879-0380
[Journal-full-title]
Current opinion in genetics & development
[ISO-abbreviation]
Curr. Opin. Genet. Dev.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
51
48.
Capurso G, Crnogorac-Jurcevic T, Milione M, Panzuto F, Campanini N, Dowen SE, Di Florio A, Sette C, Bordi C, Lemoine NR, Delle Fave G:
Peanut-like 1 (septin 5) gene expression in normal and neoplastic human endocrine pancreas.
Neuroendocrinology
; 2005;81(5):311-21
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[Title]
Peanut-like 1 (septin 5) gene expression in normal and neoplastic human
endocrine pancreas
.
As the secretory apparatus of pancreatic islet cells closely resembles that of neurons, we decided to study the expression of PNUTL1 in the human
endocrine pancreas
, both in normal
islets
and in pancreatic
endocrine
tumors (PETs).
Normal pancreatic tissue, purified
islets
, 11 PETs and two cell lines were used to evaluate the presence of PNUTL1 by RT-PCR and Western blot.
The expression of the PNUTL1 protein was also evaluated by immunohistochemistry on normal
pancreas
, additional 26 PETs, eight pancreatic adenocarcinomas, one mixed
endocrine
-exocrine pancreatic
neoplasm
, a specimen of solid papillary pseudomucinous
tumor
, an adult islet cell hyperplasia and a case of neonatal nesidioblastosis.
In addition, a tissue array (LandMark High Density Cancer Tissue MicroArray) comprising 280 various
tumor
and matched normal specimens was utilized.
In the normal
pancreas
PNUTL1 expression is almost exclusively confined to the islet cells, weak expression was occasionally seen in some acinar cells, while immunoreactivity was completely absent in the ductal epithelia.
Our findings describe for the first time the high expression levels of PNUTL1 in human pancreatic
endocrine
cells that suggests a similar role of this protein in islet cells to that demonstrated in neuronal tissues, and warrants further functional studies of this protein.
[MeSH-major]
Cell Cycle Proteins / metabolism. Gene Expression / physiology. Gene Expression Regulation, Neoplastic / physiology.
Islets
of
Langerhans
/ metabolism. Pancreatic Neoplasms / metabolism
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[Copyright]
Copyright (c) 2005 S. Karger AG, Basel.
(PMID = 16179808.001).
[ISSN]
0028-3835
[Journal-full-title]
Neuroendocrinology
[ISO-abbreviation]
Neuroendocrinology
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / RNA, Messenger; EC 3.6.1.- / SEPT5 protein, human; EC 3.6.1.- / Septins
49.
Zhang Q, Davenport JR, Croyle MJ, Haycraft CJ, Yoder BK:
Disruption of IFT results in both exocrine and endocrine abnormalities in the pancreas of Tg737(orpk) mutant mice.
Lab Invest
; 2005 Jan;85(1):45-64
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[Title]
Disruption of IFT results in both exocrine and
endocrine
abnormalities in the
pancreas of
Tg737(orpk) mutant mice.
Here, we further establish a connection between cilia dysfunction and disease by showing that loss of polaris (Tg737), an intraflagellar transport (IFT) protein required for ciliogenesis, causes abnormalities in the exocrine and
endocrine pancreas
of the Tg737(orpk) mouse.
In addition, serum amylase levels are elevated and carboxypeptidase is abnormally activated within the
pancreas
.
Intriguingly, although the acini are severely affected in Tg737(orpk) mutants, cilia and Tg737 expression are restricted to the ducts and
islets
and are not detected on acinar cells.
Analysis of the
endocrine pancreas
in Tg737(orpk) mutants revealed normal differentiation and distribution of cell types in the
islets
.
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(PMID = 15580285.001).
[ISSN]
0023-6837
[Journal-full-title]
Laboratory investigation; a journal of technical methods and pathology
[ISO-abbreviation]
Lab. Invest.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / P30 DK074038; United States / NIDDK NIH HHS / DK / DK07545; United States / NIDDK NIH HHS / DK / R01 DK65655
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Tg737Rpw protein, mouse; 0 / Tumor Suppressor Proteins; EC 3.2.1.23 / beta-Galactosidase
50.
Jain R, Lammert E:
Cell-cell interactions in the endocrine pancreas.
Diabetes Obes Metab
; 2009 Nov;11 Suppl 4:159-67
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[Title]
Cell-cell interactions in the
endocrine pancreas
.
The
islets
of
Langerhans
forming the
endocrine pancreas
are composed of alpha-, beta-, delta-, epsilon- and PP-cells, and interactions between these cells are required for fine-tuning glucose homeostasis of the body.
The
endocrine
cells communicate through homotypic or heterotypic cell-cell adhesion, or in a paracrine fashion, and this communication is involved in the regulated secretion of islet hormones.
This review discusses how islet hormones, secreted molecules and ions influence the
endocrine
cells and how cell adhesion molecules such as neural cell adhesion molecule, cadherins, connexin-36, Eph receptors and ephrin ligands, as well as extracellular matrix proteins, modulate pancreatic islet function.
[MeSH-major]
Cell Communication / physiology. Insulin-Secreting Cells / physiology.
Islets
of
Langerhans
/ cytology. Neural Cell Adhesion Molecules / physiology. Receptors, Eph Family / physiology
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(PMID = 19817798.001).
[ISSN]
1463-1326
[Journal-full-title]
Diabetes, obesity & metabolism
[ISO-abbreviation]
Diabetes Obes Metab
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Neural Cell Adhesion Molecules; EC 2.7.10.1 / Receptors, Eph Family
51.
Reis AF, Hauache OM, Velho G:
Vitamin D endocrine system and the genetic susceptibility to diabetes, obesity and vascular disease. A review of evidence.
Diabetes Metab
; 2005 Sep;31(4 Pt 1):318-25
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[Title]
Vitamin D
endocrine
system and the genetic susceptibility to diabetes, obesity and vascular disease. A review of evidence.
The Vitamin D
endocrine
system regulates multiple aspects of calcium metabolism and cellular differentiation and replication in the immune system,
endocrine pancreas
, liver, skeletal muscles and adipocytes.
[MeSH-major]
Diabetes Mellitus / genetics.
Endocrine
System / physiology. Genetic Predisposition to Disease. Obesity / genetics. Receptors, Calcitriol / genetics. Vascular Diseases / genetics. Vitamin D / physiology
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(PMID = 16369193.001).
[ISSN]
1262-3636
[Journal-full-title]
Diabetes & metabolism
[ISO-abbreviation]
Diabetes Metab.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D
[Number-of-references]
79
52.
Lavoie EG, Fausther M, Kauffenstein G, Kukulski F, Künzli BM, Friess H, Sévigny J:
Identification of the ectonucleotidases expressed in mouse, rat, and human Langerhans islets: potential role of NTPDase3 in insulin secretion.
Am J Physiol Endocrinol Metab
; 2010 Oct;299(4):E647-56
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[Title]
Identification of the ectonucleotidases expressed in mouse, rat, and human
Langerhans islets
: potential role of NTPDase3 in insulin secretion.
Extracellular nucleotides and adenosine regulate
endocrine
pancreatic functions such as insulin secretion by
Langerhans
islet β-cells via the activation of specific P2 and P1 receptors.
The objective of this study was to identify and localize the major ectonucleotidases, namely NTPDases and ecto-5'-nucleotidase, present in the
endocrine pancreas
.
The localization of ectonucleotidase activity and protein was carried out in situ by enzyme histochemistry and immunolocalization in mouse, rat, and human
pancreas
sections.
NTPDase1 was localized in all blood vessels and acini, and NTPDase2 was localized in capillaries of
Langerhans islets
and in peripheral conjunctive tissue, whereas NTPDase3 was detected in all
Langerhans
islet cell types.
Interestingly, among the mammalian species tested, ecto-5'-nucleotidase was present only in rat
Langerhans
islet cells, where it was coexpressed with NTPDase3.
In conclusion, all pancreatic
endocrine
cells express NTPDase3 that was shown to modulate insulin secretion in rat INS-1 (832/13) β-cells.
Ecto-5'-nucleotidase is expressed in rat
Langerhans
islet cells but absent in human and mouse
endocrine
cells.
[MeSH-major]
5'-Nucleotidase / physiology. Insulin / secretion.
Islets
of
Langerhans
/ enzymology.
Islets
of
Langerhans
/ secretion. Pyrophosphatases / physiology
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(PMID = 20682839.001).
[ISSN]
1522-1555
[Journal-full-title]
American journal of physiology. Endocrinology and metabolism
[ISO-abbreviation]
Am. J. Physiol. Endocrinol. Metab.
[Language]
eng
[Grant]
Canada / Canadian Institutes of Health Research / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Insulin; EC 3.1.3.5 / 5'-Nucleotidase; EC 3.6.1.- / Pyrophosphatases; EC 3.6.1.- / nucleoside-triphosphate diphosphohydrolase 3
53.
Saruç M, Karaarslan M, Rasa K, Saygili O, Ince U, Baysal C, Pour PM, Cakmakçi M, Tözün N:
Pancreatic cancer and glucose metabolism.
Turk J Gastroenterol
; 2009 Dec;20(4):257-60
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We aimed to investigate the relationship between diabetes and pancreatic cancer, and also the impact
of tumor
removal on glucose metabolism.
Thirteen patients (72%) had normal glucose metabolism after
tumor
removal.
CONCLUSIONS: Our results showed that
tumor
removal in pancreatic cancer patients improved glucose metabolism.
This occurred despite a postoperative reduction in
endocrine pancreas
mass, which may suggest the presence of insulin resistance and diabetogenic effect of pancreatic cancer.
The elucidation of the mechanism is of immense importance for providing an early
tumor
marker and preventative and therapeutic modalities.
[MeSH-minor]
Aged. Aged, 80 and over. Biomarkers,
Tumor
. Diabetes Mellitus / epidemiology. Diabetes Mellitus / metabolism. Female. Glucose Tolerance Test. Humans. Hyperinsulinism / epidemiology. Hyperinsulinism / metabolism. Insulin / blood. Insulin Resistance. Male. Middle Aged. Postoperative Period. Risk Factors
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(PMID = 20084568.001).
[ISSN]
2148-5607
[Journal-full-title]
The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology
[ISO-abbreviation]
Turk J Gastroenterol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Turkey
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Blood Glucose; 0 / Insulin
54.
Reusens B, Remacle C:
Programming of the endocrine pancreas by the early nutritional environment.
Int J Biochem Cell Biol
; 2006;38(5-6):913-22
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[Title]
Programming of the
endocrine pancreas
by the early nutritional environment.
It focuses on the alteration of the
endocrine pancreas
at birth.
[MeSH-major]
Pancreas
/ embryology. Prenatal Exposure Delayed Effects
[MeSH-minor]
Animals. Diabetes, Gestational / physiopathology. Female. Humans. Insulin-Secreting Cells / pathology.
Islets
of
Langerhans
/ embryology. Mitochondria / physiology. Pregnancy. Protein Deficiency / complications. Protein-Energy Malnutrition / complications. Uterus / blood supply
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(PMID = 16337425.001).
[ISSN]
1357-2725
[Journal-full-title]
The international journal of biochemistry & cell biology
[ISO-abbreviation]
Int. J. Biochem. Cell Biol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Number-of-references]
66
55.
Rieck S, Kaestner KH:
Expansion of beta-cell mass in response to pregnancy.
Trends Endocrinol Metab
; 2010 Mar;21(3):151-8
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During times of prolonged metabolic demand for insulin, the
endocrine pancreas
can respond by increasing beta-cell mass, both by increasing cell size and by changing the balance between beta-cell proliferation and apoptosis.
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[Copyright]
Copyright 2009 Elsevier Ltd. All rights reserved.
[Cites]
Diabetes. 2002 Jun;51(6):1793-804
[
12031967.001
]
[Cites]
Mol Endocrinol. 2002 Jun;16(6):1394-406
[
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(PMID = 20015659.001).
[ISSN]
1879-3061
[Journal-full-title]
Trends in endocrinology and metabolism: TEM
[ISO-abbreviation]
Trends Endocrinol. Metab.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK055342-02; United States / NIDDK NIH HHS / DK / R01 DK055342; United States / NIDDK NIH HHS / DK / R01 DK055342-02; United States / NIDDK NIH HHS / DK / R01-DK055243
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
84
[Other-IDs]
NLM/ NIHMS309330; NLM/ PMC3627215
56.
Yagil C, Barkalifa R, Sapojnikov M, Wechsler A, Ben-Dor D, Weksler-Zangen S, Kaiser N, Raz I, Yagil Y:
Metabolic and genomic dissection of diabetes in the Cohen rat.
Physiol Genomics
; 2007 Apr 24;29(2):181-92
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The development of diabetes is accompanied by depletion of the acini from the exocrine
pancreas
and replacement with fat cells, while the appearance of the
islets
of
Langerhans
remains intact.
With reversion back from diabetogenic to regular diet, the diabetic phenotype disappears but the histological changes in the exocrine
pancreas
prevail.
We conclude that the development of diabetes in our model is dependent upon high casein and low copper in diet, that it is accompanied by histomorphological changes in the exocrine but not
endocrine pancreas
, that it is reversible, and that it is associated with a major QTL on chromosome 4 in which we detected Ica1, a high priority candidate gene.
[MeSH-major]
Animal Feed / analysis. Diabetes Mellitus, Experimental / genetics. Diabetes Mellitus, Experimental / metabolism. Diet. Disease Models, Animal.
Pancreas
/ pathology. Quantitative Trait Loci
Hazardous Substances Data Bank.
COPPER, ELEMENTAL
.
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(PMID = 17213368.001).
[ISSN]
1531-2267
[Journal-full-title]
Physiological genomics
[ISO-abbreviation]
Physiol. Genomics
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Autoantigens; 0 / Caseins; 0 / Ica1 protein, rat; 789U1901C5 / Copper
57.
Palumbo P, De Gaetano A:
An islet population model of the endocrine pancreas.
J Math Biol
; 2010 Aug;61(2):171-205
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[Title]
An islet population model of the
endocrine pancreas
.
Without detailing the chain of biochemical events giving rise to the delivery of insulin packets, the effect of the
islets
' bursting response to varying glucose concentration is described by a simple second order nonlinear model, of the same functional form for all
islets
, but with a random distribution of parameter values over the one million
islets
considered.
[MeSH-major]
Islets
of
Langerhans
/ cytology.
Islets
of
Langerhans
/ metabolism. Models, Biological
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[ISSN]
1432-1416
[Journal-full-title]
Journal of mathematical biology
[ISO-abbreviation]
J Math Biol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Blood Glucose; 0 / Insulin
58.
Hammerman MR:
Growing new endocrine pancreas in situ.
Clin Exp Nephrol
; 2006 Mar;10(1):1-7
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[Title]
Growing new
endocrine pancreas
in situ.
Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective
endocrine
differentiation in situ and normalize glucose tolerance.
[MeSH-major]
Organogenesis.
Pancreas
/ embryology.
Pancreas
, Artificial. Tissue Engineering / methods
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Ann Med. 2001 Apr;33(3):186-92
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]
(PMID = 16544171.001).
[ISSN]
1342-1751
[Journal-full-title]
Clinical and experimental nephrology
[ISO-abbreviation]
Clin. Exp. Nephrol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Japan
[Number-of-references]
24
59.
Deramaudt TB, Sachdeva MM, Wescott MP, Chen Y, Stoffers DA, Rustgi AK:
The PDX1 homeodomain transcription factor negatively regulates the pancreatic ductal cell-specific keratin 19 promoter.
J Biol Chem
; 2006 Dec 15;281(50):38385-95
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The
pancreas
has three distinct cell types, ductal, acinar, and islet, each with different functions.
Embryologically, the pancreatic and duodenal homeobox 1 (PDX1) homeodomain protein is critical for the initiation of all pancreatic lineages; however, the later differentiation of the
endocrine pancreas
is uniquely dependent upon high PDX1 expression, whereas PDX1 is down-regulated in the ductal and acinar cell lineages.
Furthermore, PDX1 may inhibit the ductal differentiation program in the pancreatic
endocrine
compartment, particularly beta cells.
[MeSH-major]
Homeodomain Proteins / physiology. Keratin-19 / genetics.
Pancreas
/ metabolism. Promoter Regions, Genetic. Trans-Activators / physiology
[MeSH-minor]
Animals. Base Sequence. Cell Line. DNA Primers. Genes, Reporter. Insulinoma / genetics. Insulinoma / pathology. Mice.
Neoplasm
Proteins / physiology
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.
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(subscription/membership/fee required).
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Mouse Genome Informatics (MGI)
.
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(PMID = 17056599.001).
[ISSN]
0021-9258
[Journal-full-title]
The Journal of biological chemistry
[ISO-abbreviation]
J. Biol. Chem.
[Language]
eng
[Grant]
United States / NIGMS NIH HHS / GM / 5T32 GM 08216-19; United States / NIDDK NIH HHS / DK / P01 DK 49210; United States / NIDDK NIH HHS / DK / P30 DK 19525; United States / NIDDK NIH HHS / DK / P30 DK 50306; United States / NIDDK NIH HHS / DK / R01 DK 068157; United States / NIDDK NIH HHS / DK / R01 DK 50306
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA Primers; 0 / Homeodomain Proteins; 0 / Keratin-19; 0 / Neoplasm Proteins; 0 / Trans-Activators; 0 / myeloid ecotropic viral integration site 1 protein; 0 / pancreatic and duodenal homeobox 1 protein
60.
Erbel S, Reers C, Nawroth PP, Ritzel RA:
Prolonged culture of human islets induces ER stress.
Exp Clin Endocrinol Diabetes
; 2010 Feb;118(2):81-6
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[Title]
Prolonged culture of human
islets
induces ER stress.
Isolated human
islets
are a frequently used model to examine islet pathophysiology in T2D.
Therefore it is important to establish how function and beta-cell turnover of human
islets
change in culture.
Islets
from four organ donors were cultured over four weeks.
At 0, 1, 2, 3 and 4 weeks aliquots of
islets
were used for analysis of a) islet-cell turnover (replication by Ki-67 and apoptosis by TUNEL staining), b) the ER stress level (CHOP and phospho-eIF2alpha staining), c) fractional beta-cell content (insulin staining) and d) islet function (2 h static incubation).
In comparison to
islets
in situ islet cell turnover is accelerated (>10-fold).
In conclusion, isolated human
islets
may be used for in vitro experiments for up to three weeks.
Studies analyzing the pathophysiology of human T2D at the level of the
endocrine pancreas
need to confirm results obtained with isolated human
islets
by analysis of primary human pancreatic tissue.
[MeSH-major]
Apoptosis / physiology. Endoplasmic Reticulum / metabolism.
Islets
of
Langerhans
/ cytology.
Islets
of
Langerhans
/ metabolism
NCI CPTC Antibody Characterization Program.
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[Copyright]
J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart. New York.
(PMID = 19838981.001).
[ISSN]
1439-3646
[Journal-full-title]
Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
[ISO-abbreviation]
Exp. Clin. Endocrinol. Diabetes
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Eukaryotic Initiation Factor-2; 0 / Insulin; 147336-12-7 / Transcription Factor CHOP
61.
Bindom SM, Lazartigues E:
The sweeter side of ACE2: physiological evidence for a role in diabetes.
Mol Cell Endocrinol
; 2009 Apr 29;302(2):193-202
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The enzyme is present in the kidney, liver, adipose tissue and
pancreas
.
Its expression is elevated in the
endocrine pancreas
in diabetes and in the early phase during diabetic nephropathy.
Recently, we have shown the presence of the Mas receptor in the mouse
pancreas
and observed a reduction in Mas receptor immuno-reactivity as well as higher fasting blood glucose levels in ACE2 knockout mice, indicating that these mice may be a new model to study the role of ACE2 in diabetes.
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(PMID = 18948167.001).
[ISSN]
1872-8057
[Journal-full-title]
Molecular and cellular endocrinology
[ISO-abbreviation]
Mol. Cell. Endocrinol.
[Language]
ENG
[Grant]
United States / NCRR NIH HHS / RR / RR018766-066843; United States / NCRR NIH HHS / RR / P20 RR018766-066843; United States / NINDS NIH HHS / NS / R21 NS052479; United States / NINDS NIH HHS / NS / R21 NS052479-02S1; United States / NINDS NIH HHS / NS / NS052479-01S1; United States / NCRR NIH HHS / RR / P20 RR018766-057611; United States / NINDS NIH HHS / NS / R21 NS052479-01S1; United States / NINDS NIH HHS / NS / NS052479; United States / NINDS NIH HHS / NS / NS052479-02S1; United States / NCRR NIH HHS / RR / P20 RR018766; United States / NCRR NIH HHS / RR / RR018766-057611
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
Ireland
[Chemical-registry-number]
0 / Peptide Fragments; 0 / Proto-Oncogene Proteins; 0 / Receptors, G-Protein-Coupled; 0 / angiotensin I (1-7); 0 / proto-oncogene proteins c-mas-1; 9041-90-1 / Angiotensin I; EC 3.4.15.1 / Peptidyl-Dipeptidase A; EC 3.4.17.- / angiotensin converting enzyme 2
[Number-of-references]
144
[Other-IDs]
NLM/ NIHMS106716; NLM/ PMC2676688
62.
Nikolic T, Geutskens SB, van Rooijen N, Drexhage HA, Leenen PJ:
Dendritic cells and macrophages are essential for the retention of lymphocytes in (peri)-insulitis of the nonobese diabetic mouse: a phagocyte depletion study.
Lab Invest
; 2005 Apr;85(4):487-501
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Dendritic cells (DC) and macrophages (Mphi) are present in high numbers in the
pancreas of
the non-obese diabetic (NOD) mouse during the diabetogenic process from very early stages onwards.
Interestingly, this treatment caused a delayed disappearance (7-21 days postinjection) of DC and Mphi from the
endocrine pancreas
at a time when monocytes, DC and Mphi had already repopulated the circulation and the spleen.
The depletion of DC and Mphi from the
endocrine pancreas
was accompanied by a total disappearance of lymphocytes from the
pancreas
.
Taken together, our data show an essential role of phagocytic cells, that is, DC and Mphi, in the recruitment of lymphocytes to the pancreatic
islets
in NOD mice.
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(PMID = 15654358.001).
[ISSN]
0023-6837
[Journal-full-title]
Laboratory investigation; a journal of technical methods and pathology
[ISO-abbreviation]
Lab. Invest.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
63.
Wilson CG, Schupp M, Burkhardt BR, Wu J, Young RA, Wolf BA:
Liver-specific overexpression of pancreatic-derived factor (PANDER) induces fasting hyperglycemia in mice.
Endocrinology
; 2010 Nov;151(11):5174-84
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The
pancreas
-derived hormones, insulin and glucagon, are the two main regulators of glucose homeostasis.
Pancreatic-derived factor (PANDER) is a novel cytokine-like molecule secreted from the
endocrine pancreas
, but its biological function is currently unknown.
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(PMID = 20844005.001).
[ISSN]
1945-7170
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / K01 DK070744; United States / NIDDK NIH HHS / DK / K01-DK070744
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Blood Glucose; 0 / Culture Media, Conditioned; 0 / Cyclic AMP Response Element-Binding Protein; 0 / Cytokines; 0 / Insulin; 0 / PANDER protein, mouse; E0399OZS9N / Cyclic AMP
[Other-IDs]
NLM/ PMC2954722
64.
Ghanassia E, Brun JF, Mercier J, Raynaud E:
Oxidative mechanisms at rest and during exercise.
Clin Chim Acta
; 2007 Aug;383(1-2):1-20
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In the classic model, three main organs/tissues for substrate fluxes (liver, adipose tissue and skeletal muscle) and one organ regulating main reactions by adaptation of hormonal secretions (
endocrine pancreas
) are described.
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(PMID = 17544388.001).
[ISSN]
0009-8981
[Journal-full-title]
Clinica chimica acta; international journal of clinical chemistry
[ISO-abbreviation]
Clin. Chim. Acta
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Netherlands
[Number-of-references]
122
65.
Peschke E, Frese T, Chankiewitz E, Peschke D, Preiss U, Schneyer U, Spessert R, Mühlbauer E:
Diabetic Goto Kakizaki rats as well as type 2 diabetic patients show a decreased diurnal serum melatonin level and an increased pancreatic melatonin-receptor status.
J Pineal Res
; 2006 Mar;40(2):135-43
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There are functional inter-relationships between the beta cells of the
endocrine pancreas
and the pineal gland, where the synchronizing circadian molecule melatonin originates.
Diabetic patients showed a decrease in melatonin levels, while in the
pancreas of
GK rats an upregulation of the melatonin-receptor mRNA was determined.
The pancreatic
islets
of GK rats showed expression of the mRNA for the pancreatic melatonin (MT1) receptor, which had previously been identified in rats and insulinoma (INS1) cells.
Besides their presence in animal cells, the MT1-receptor transcript was also detected in human
pancreas
by RT-PCR.
[MeSH-major]
Diabetes Mellitus, Type 2 / metabolism. Insulin / blood. Melatonin / blood.
Pancreas
/ metabolism. Receptors, Melatonin / metabolism
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MELATONIN
.
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(PMID = 16441550.001).
[ISSN]
0742-3098
[Journal-full-title]
Journal of pineal research
[ISO-abbreviation]
J. Pineal Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Insulin; 0 / Receptors, Melatonin; EC 2.3.1.87 / Arylalkylamine N-Acetyltransferase; EC 2.7.10.1 / Receptor, Insulin; JL5DK93RCL / Melatonin
66.
Li Z, Korzh V, Gong Z:
DTA-mediated targeted ablation revealed differential interdependence of endocrine cell lineages in early development of zebrafish pancreas.
Differentiation
; 2009 Nov;78(4):241-52
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[Title]
DTA-mediated targeted ablation revealed differential interdependence
of endocrine
cell lineages in early development of zebrafish
pancreas
.
In order to study the zebrafish
endocrine pancreas
cell lineage, transgenic expression of diphtheria toxin gene A chain (DTA) under two cell type-specific promoters derived from the insulin (ins) and somatostatin2 (sst2) genes was used to ablate the two types
of endocrine
cells: insulin-producing beta-cells and somatostatin-producing delta-cells, respectively.
Ablation of delta-cells led to reduction of all three types
of endocrine
cells: alpha-, beta-, and delta.
By taking advantage of Tg(ins:gfp) and Tg(sst2:gfp) lines, we also monitored the changes of different types
of endocrine
cells in vivo after ablation and found that both beta- and delta-cell populations significantly recovered by 3dpf after their ablation and it seemed that delta-cells had a better capability of recovery than beta-cells.
[MeSH-major]
Glucagon-Secreting Cells / metabolism.
Islets
of
Langerhans
/ cytology.
Pancreas
/ cytology. Somatostatin-Secreting Cells / metabolism. Zebrafish / genetics
ZFIN.
ZFIN
.
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(PMID = 19553000.001).
[ISSN]
1432-0436
[Journal-full-title]
Differentiation; research in biological diversity
[ISO-abbreviation]
Differentiation
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Diphtheria Toxin; 0 / Insulin; 0 / Peptide Fragments; 0 / diphtheria toxin fragment A; 147336-22-9 / Green Fluorescent Proteins; 51110-01-1 / Somatostatin
67.
Oue N, Mitani Y, Aung PP, Sakakura C, Takeshima Y, Kaneko M, Noguchi T, Nakayama H, Yasui W:
Expression and localization of Reg IV in human neoplastic and non-neoplastic tissues: Reg IV expression is associated with intestinal and neuroendocrine differentiation in gastric adenocarcinoma.
J Pathol
; 2005 Oct;207(2):185-98
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Insulin-producing beta cells of the
endocrine pancreas
were positive for Reg IV.
No association was found between Reg IV expression and clinical characteristics such as
tumour
stage and patient prognosis.
Of 36 colorectal adenocarcinomas, 13 (36.1%) were positive for Reg IV, which was associated with
tumour
stage (p = 0.0379, Fisher's exact test).
Reg IV expression was also detected in 5 (21.7%) of 23 ductal adenocarcinomas of the
pancreas
.
[MeSH-major]
Adenocarcinoma / chemistry. Lectins, C-Type / analysis.
Neoplasm
Proteins / analysis. Stomach Neoplasms / chemistry
[MeSH-minor]
Adenoma / chemistry. Biomarkers,
Tumor
/ analysis. Blotting, Western / methods. Breast Neoplasms / chemistry. Carcinoid
Tumor
/ chemistry. Cell Differentiation / physiology. Cell Line,
Tumor
. Colon / metabolism. Colorectal Neoplasms / chemistry. Female. Humans. Immunohistochemistry / methods. Intestine, Small / metabolism. Lung Neoplasms / chemistry.
Pancreas
/ metabolism. Pancreatic Neoplasms / chemistry. Phenotype. RNA, Messenger / analysis. RNA,
Neoplasm
/ analysis. Reverse Transcriptase Polymerase Chain Reaction / methods. Stomach / metabolism
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[Copyright]
Copyright (c) 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
(PMID = 16086444.001).
[ISSN]
0022-3417
[Journal-full-title]
The Journal of pathology
[ISO-abbreviation]
J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Lectins, C-Type; 0 / Neoplasm Proteins; 0 / REG4 protein, human; 0 / RNA, Messenger; 0 / RNA, Neoplasm
68.
Rindi G, Solcia E:
Endocrine hyperplasia and dysplasia in the pathogenesis of gastrointestinal and pancreatic endocrine tumors.
Gastroenterol Clin North Am
; 2007 Dec;36(4):851-65, vi
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[Title]
Endocrine
hyperplasia and dysplasia in the pathogenesis of gastrointestinal and pancreatic
endocrine
tumors.
Non-neoplastic proliferative lesions
of endocrine
cells have been described throughout the gastrointestinal tract and
pancreas
.
A multistep continuum from hyperplasia and dysplasia to
neoplasia
originally was identified and systematically defined for histamine-producing enterochromaffin-like (ECL) cells of the gastric corpus.
Preneoplastic lesions of the
endocrine pancreas
still lack a solid and widely accepted definition of a multistep growth process.
Similarly, in spite of reports of carcinoid-associated
endocrine
cell hyperplasia, there is no systematic definition of nonneoplastic lesions of the
endocrine
cells of the ileum, appendix and colorectum.
[MeSH-minor]
Diagnosis
, Differential. Humans. Hyperplasia / pathology. Risk Factors
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(PMID = 17996794.001).
[ISSN]
0889-8553
[Journal-full-title]
Gastroenterology clinics of North America
[ISO-abbreviation]
Gastroenterol. Clin. North Am.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
80
69.
Buono S, Odierna G 2nd, Putti R:
Morphology of the pancreas of some species belonging to the genera Phelsuma and Gecko (family Gekkonidae): evidence of apoptotic process during the seasonal cycle.
Anat Embryol (Berl)
; 2006 Oct;211(5):413-21
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[Title]
Morphology of the
pancreas of
some species belonging to the genera Phelsuma and Gecko (family Gekkonidae): evidence of apoptotic process during the seasonal cycle.
In this study we investigated comparative morphology of the
endocrine pancreas
of several species belonging to the family Gekkonidae and apoptotic processes of the
pancreas
which may be correlated to the seasonal cycle.
In all these species the
pancreas
consisted of large and medium
islets
as well as
endocrine
cells which were scattered throughout the acinar cells.
Four mayor cell types were identified in the
endocrine pancreas
, using immunocytochemistry: glucagon-immunoreactive (A) cells, insulin-immunoreactive (B) cells, somatostatin-immunoreactive (D) cells, and pancreatic polypeptide immunoreactive (PP) cells.
In the
endocrine pancreas
the amount of A cells and B cells was either equal or a prevalence of A cells was observed.
The animals belonging to the genus Phelsuma taken in the dry season (July) showed numerous vacuolated, Caspase 3, 9 and 11-immunoreactive acinar and some
endocrine
cells containing picnotic nuclei which were positive to tunel reaction.
The animals belonging to the genus Gekko taken at the
end
of the dry season (October) exhibited strongly vacuolated, Caspase 3, 9 and 11-immunoreactive
endocrine
and some acinar cells containing nuclei which were positive to tunel reaction.
[MeSH-major]
Adaptation, Physiological. Apoptosis / physiology. Lizards / physiology.
Pancreas
/ cytology. Seasons
[MeSH-minor]
Animals. Caspases / metabolism. Immunohistochemistry. In Situ Nick-
End
Labeling. Species Specificity. Starvation / pathology. Starvation / physiopathology. Tropical Climate
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(PMID = 16763810.001).
[ISSN]
0340-2061
[Journal-full-title]
Anatomy and embryology
[ISO-abbreviation]
Anat. Embryol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
EC 3.4.22.- / Caspases
70.
Bibliography. Current world literature. Diabetes and the endocrine pancreas.
Curr Opin Endocrinol Diabetes Obes
; 2008 Apr;15(2):193-207
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[Title]
Bibliography. Current world literature. Diabetes and the
endocrine pancreas
.
[MeSH-major]
Diabetes Mellitus / physiopathology.
Islets
of
Langerhans
/ physiopathology
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(PMID = 18316957.001).
[ISSN]
1752-2978
[Journal-full-title]
Current opinion in endocrinology, diabetes, and obesity
[ISO-abbreviation]
Curr Opin Endocrinol Diabetes Obes
[Language]
eng
[Publication-type]
Bibliography
[Publication-country]
England
71.
Lyttle BM, Li J, Krishnamurthy M, Fellows F, Wheeler MB, Goodyer CG, Wang R:
Transcription factor expression in the developing human fetal endocrine pancreas.
Diabetologia
; 2008 Jul;51(7):1169-80
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[Title]
Transcription factor expression in the developing human fetal
endocrine pancreas
.
AIMS/HYPOTHESIS: Morphological changes that occur during pancreatic
endocrine
cell differentiation have been shown in rodent systems to be dependent on sequential alterations in transcription factor expression.
METHODS: Human fetal
pancreases
were examined at early (8-12 weeks of fetal age), middle (14-16 weeks) and late (19-21 weeks) stages, using immunohistological, microarray and qRT-PCR analyses.
Given that neurogenin 3 (NGN3) expression is critical for establishing the
endocrine
cell programme in the rodent
pancreas
, we examined its expression pattern and co-localisation in PDX-1(+), insulin(+) and glucagon(+) cells.
Our microarray and co-localisation analyses of transcription factors linked to NGN3 demonstrated that ISL1 transcription factor (ISL1), neurogenic differentiation 1 (NEUROD1), NK2 related transcription factor related, locus 2 (NKX2-2) and paired box gene 6 (PAX6) were upregulated during development and present in all four
endocrine
cell types, while NK6 related transcription factor related, locus 1 (NKX6-1) was expressed exclusively in beta cells.
CONCLUSIONS/INTERPRETATION: This study is an important step towards identifying key molecular factors involved in development of the human fetal
endocrine pancreas
.
[MeSH-major]
Gene Expression Profiling. Gene Expression Regulation, Developmental.
Pancreas
/ embryology.
Pancreas
/ physiology. Transcription Factors / genetics
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[ISSN]
0012-186X
[Journal-full-title]
Diabetologia
[ISO-abbreviation]
Diabetologia
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / Biomarkers; 0 / FOXA2 protein, human; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Hepatocyte Nuclear Factor 6; 0 / Homeodomain Proteins; 0 / MNX1 protein, human; 0 / NEUROG3 protein, human; 0 / Nerve Tissue Proteins; 0 / Nkx-2.2 homedomain protein; 0 / ONECUT1 protein, human; 0 / PAX4 protein, human; 0 / Paired Box Transcription Factors; 0 / Snail Family Transcription Factors; 0 / Trans-Activators; 0 / Transcription Factors; 0 / pancreatic and duodenal homeobox 1 protein; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta
72.
Bibliography. Current world literature. Diabetes and the endocrine pancreas.
Curr Opin Endocrinol Diabetes Obes
; 2007 Apr;14(2):170-96
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[Title]
Bibliography. Current world literature. Diabetes and the
endocrine pancreas
.
[MeSH-major]
Diabetes Mellitus.
Islets
of
Langerhans
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(PMID = 17940437.001).
[ISSN]
1752-2978
[Journal-full-title]
Current opinion in endocrinology, diabetes, and obesity
[ISO-abbreviation]
Curr Opin Endocrinol Diabetes Obes
[Language]
eng
[Publication-type]
Bibliography
[Publication-country]
England
73.
Lee JS, Cho WJ, Jeftinija K, Jeftinija S, Jena BP:
Porosome in astrocytes.
J Cell Mol Med
; 2009 Feb;13(2):365-72
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In the past decade, porosomes have been determined to be the universal secretory machinery in cells, present in the exocrine
pancreas
,
endocrine
and neuroendocrine cells, and in neurons.
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(PMID = 18400049.001).
[ISSN]
1582-4934
[Journal-full-title]
Journal of cellular and molecular medicine
[ISO-abbreviation]
J. Cell. Mol. Med.
[Language]
ENG
[Grant]
United States / NINDS NIH HHS / NS / R01 NS039918; United States / NINDS NIH HHS / NS / NS39918
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
England
[Chemical-registry-number]
0 / Snap23 protein, rat; 0 / Snap25 protein, rat; 0 / Synaptosomal-Associated Protein 25; 0 / Vesicular Transport Proteins
[Other-IDs]
NLM/ PMC3823362
74.
Anderson LL:
Discovery of the 'porosome'; the universal secretory machinery in cells.
J Cell Mol Med
; 2006 Jan-Mar;10(1):126-31
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The release of neurotransmitters at the nerve terminal for neurotransmission, release of insulin from beta-cells of the
endocrine pancreas
for regulating blood glucose levels, the release of growth hormone from GH cells of the pituitary gland to regulate body growth, or the expulsion of zymogen from exocrine
pancreas
to digest food, are only a few examples of key physiological processes made possible by cell secretion.
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(PMID = 16563225.001).
[ISSN]
1582-1838
[Journal-full-title]
Journal of cellular and molecular medicine
[ISO-abbreviation]
J. Cell. Mol. Med.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Romania
[Chemical-registry-number]
0 / MADS Domain Proteins; 0 / MEF2 Transcription Factors; 0 / MEF2A protein, human; 0 / Myogenic Regulatory Factors; 0 / Protein Inhibitors of Activated STAT; 0 / SUMO-1 Protein; EC 6.3.2.19 / Ubiquitin-Protein Ligases; K3Z4F929H6 / Lysine
[Number-of-references]
37
[Other-IDs]
NLM/ PMC3933105
75.
Leoni L, Roman BB:
MR imaging of pancreatic islets: tracking isolation, transplantation and function.
Curr Pharm Des
; 2010 May;16(14):1582-94
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[Title]
MR imaging of pancreatic
islets
: tracking isolation, transplantation and function.
This review focuses on the most recent advancements in magnetic resonance imaging (MRI) of pancreatic
islets
.
In-vitro approaches aimed at characterizing the potency of isolated
islets
as well as in-vivo advancements in the assessment of transplanted beta cell mass are presented together with the significant progress made in the in-vivo imaging of the
endocrine pancreas
and islet vasculature and inflammation.
[MeSH-major]
Islets
of
Langerhans
/ pathology.
Islets
of
Langerhans
Transplantation
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consumer health - Islet Cell Transplantation
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(PMID = 20146663.001).
[ISSN]
1873-4286
[Journal-full-title]
Current pharmaceutical design
[ISO-abbreviation]
Curr. Pharm. Des.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK 001828
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Review
[Publication-country]
Netherlands
[Number-of-references]
86
76.
Simşek N, Ergün L, Ergün E, Alabay B, Ozen A:
Ultrastructure of pancreatic alpha and beta cells in young quails (Coturnix coturnix japonica) fed aflatoxin.
Dtsch Tierarztl Wochenschr
; 2007 Dec;114(12):465-9
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The present investigation was undertaken to assess the effects of aflatoxin (AF) containing diets on alpha and beta cells of the
endocrine pancreas
in young quails by means of light and electron microscopy.
Mononuclear cell infiltrates were observed in the periphery of capillaries and around
endocrine
islets
in the experimental groups.
Furthermore, capillaries of the animals in group 2 and 3 were dilated at all sides of both alpha and beta
islets
.
[MeSH-minor]
Animals. Dose-Response Relationship, Drug. Immunohistochemistry / veterinary. Microscopy, Electron / methods. Microscopy, Electron / veterinary.
Pancreas
, Exocrine / drug effects.
Pancreas
, Exocrine / ultrastructure. Random Allocation
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(PMID = 18181361.001).
[ISSN]
0341-6593
[Journal-full-title]
DTW. Deutsche tierärztliche Wochenschrift
[ISO-abbreviation]
DTW. Dtsch. Tierarztl. Wochenschr.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Aflatoxins
77.
Mercado AB, Castells S:
Pancreatic beta-cell hyperactivity in morbidly obese adolescents.
Pediatr Endocrinol Rev
; 2006 Dec;3 Suppl 4:560-3
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beta-cell hyperactivity, with increased beta-cell mass in the
pancreas
, contributes to insulin oversecretion in response to insulin resistance. beta-cell mass expansion, also known as "
endocrine pancreas
plasticity", is an adaptation to variations in insulin demand, is generally observed in obese persons and in women during late pregnancy.
Better understanding
of endocrine pancreas
plasticity and its regeneration mechanisms could lead to new treatment modalities for type 2 diabetes.
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(PMID = 17237743.001).
[ISSN]
1565-4753
[Journal-full-title]
Pediatric endocrinology reviews : PER
[ISO-abbreviation]
Pediatr Endocrinol Rev
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Israel
[Number-of-references]
32
78.
Navarro MH, Lozano MT, Agulleiro B:
Ontogeny of the endocrine pancreatic cells of the gilthead sea bream, Sparus aurata (Teleost).
Gen Comp Endocrinol
; 2006 Sep 1;148(2):213-26
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[Title]
Ontogeny of the
endocrine
pancreatic cells of the gilthead sea bream, Sparus aurata (Teleost).
The development of the gilthead sea bream, Sparus aurata,
endocrine pancreas
was studied from hatching to 114 days, using immunocytochemical techniques.
The different types
of endocrine
cells appear at distinct stages of development and differ in their arrangement.
One big islet and several small
islets
and isolated or clustered cells next to the pancreatic duct were present in 24- and 25-day-old larvae.
The
islets
were similar in cell composition to the single islet seen in the previous stage, while the isolated and grouped cells showed the coexistence of INS and diverse SSs immunoreactivities.
Nerve fibers showing PYY immunoreactivity were identified in the
islets
from 17 days onwards.
In 30- to 44-day-old larvae, GLU and NPY immunoreactivities coexisted in a few cells at the periphery of some small
islets
.
One big islet, several intermediate
islets
and numerous small
islets
were present from 51-day-old-larvae to juveniles.
GLU was colocalized with PYY and NPY in a few cells in a small peripheral area in the big islet and a few intermediate
islets
.
The outer region of small
islets
and other intermediate
islets
showed the complete coexistence of GLU, PYY, and NPY.
[MeSH-major]
Islets
of
Langerhans
/ embryology.
Islets
of
Langerhans
/ growth & development. Sea Bream / embryology. Sea Bream / growth & development
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(PMID = 16630618.001).
[ISSN]
0016-6480
[Journal-full-title]
General and comparative endocrinology
[ISO-abbreviation]
Gen. Comp. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Insulin; 0 / Neuropeptide Y; 106388-42-5 / Peptide YY; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
79.
Ardeleanu C, Arsene D, Hinescu M, Andrei F, Gutu D, Luca L, Popescu LM:
Pancreatic expression of DOG1: a novel gastrointestinal stromal tumor (GIST) biomarker.
Appl Immunohistochem Mol Morphol
; 2009 Oct;17(5):413-8
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[Title]
Pancreatic expression of DOG1: a novel gastrointestinal stromal
tumor
(GIST) biomarker.
The normal tissues showed a distinct positivity for DOG1 only in the
endocrine pancreas
, in both fetal and adult ones.
The DOG1 staining pattern in the
pancreas
islets
was granular, like that of neuroendocrine markers.
The location of DOG1 expression in pancreatic
islets
was partly similar to neuroendocrine markers chromogranin A, PGP9.5, and synaptophysin.
DOG1 positivity in fetal and adult pancreatic
islets
suggests the strong antibody affinity for neuroendocrine cells.
Before making a final conclusion regarding the suitability of DOG1 as a new neuroendocrine marker, a large survey of neuroendocrine lesions must be undertaken, including carcinoid tumors of various sites and pancreatic
endocrine
tumors.
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(PMID = 19417627.001).
[ISSN]
1533-4058
[Journal-full-title]
Applied immunohistochemistry & molecular morphology : AIMM
[ISO-abbreviation]
Appl. Immunohistochem. Mol. Morphol.
[Language]
ENG
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / ANO1 protein, human; 0 / Biomarkers, Tumor; 0 / Chloride Channels; 0 / Membrane Proteins; 0 / Neoplasm Proteins
80.
Neve B, Fernandez-Zapico ME, Ashkenazi-Katalan V, Dina C, Hamid YH, Joly E, Vaillant E, Benmezroua Y, Durand E, Bakaher N, Delannoy V, Vaxillaire M, Cook T, Dallinga-Thie GM, Jansen H, Charles MA, Clément K, Galan P, Hercberg S, Helbecque N, Charpentier G, Prentki M, Hansen T, Pedersen O, Urrutia R, Melloul D, Froguel P:
Role of transcription factor KLF11 and its diabetes-associated gene variants in pancreatic beta cell function.
Proc Natl Acad Sci U S A
; 2005 Mar 29;102(13):4807-12
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KLF11 (TIEG2) is a
pancreas
-enriched transcription factor that has elicited significant attention because of its role as negative regulator of exocrine cell growth in vitro and in vivo.
However, its functional role in the
endocrine pancreas
remains to be established.
[MeSH-major]
Cell Cycle Proteins / physiology. Diabetes Mellitus, Type 2 / genetics. Gene Expression Regulation. Insulin / metabolism.
Islets
of
Langerhans
/ physiology. Polymorphism, Genetic. Repressor Proteins / physiology. Transcription Factors / physiology
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.
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.
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.
SciCrunch.
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.
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.
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.
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[Cites]
Am J Physiol Endocrinol Metab. 2003 Dec;285(6):E1151-60
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Am J Physiol Endocrinol Metab. 2002 Aug;283(2):E217-25
[
12110525.001
]
(PMID = 15774581.001).
[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / R56 DK052913; United States / NCI NIH HHS / CA / P50 CA10270; United States / NIDDK NIH HHS / DK / R01 DK052913; United States / NIDDK NIH HHS / DK / R01 DK056620; United Kingdom / Medical Research Council / / G0000477; United States / NIDDK NIH HHS / DK / R01 DK052913-09; United States / NIDDK NIH HHS / DK / DK52913; United States / NIDDK NIH HHS / DK / DK56620
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Cell Cycle Proteins; 0 / Insulin; 0 / KLF11 protein, human; 0 / Repressor Proteins; 0 / Transcription Factors; EC 1.13.12.- / Luciferases
[Other-IDs]
NLM/ PMC554843
81.
Rafacho A, Quallio S, Ribeiro DL, Taboga SR, Paula FM, Boschero AC, Bosqueiro JR:
The adaptive compensations in endocrine pancreas from glucocorticoid-treated rats are reversible after the interruption of treatment.
Acta Physiol (Oxf)
; 2010 Nov;200(3):223-35
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[Title]
The adaptive compensations in
endocrine pancreas
from glucocorticoid-treated rats are reversible after the interruption of treatment.
Islets
from DEX rats secreted more insulin in response to increasing concentrations of glucose and other metabolic and non-metabolic stimuli, compared with that in the CTL group.
The insulin secretion for the most compounds studied returned to CTL values in DEX(10)
islets
.
Increased insulin secretion correlated well with the augmentation in β-cell proliferation and mass in DEX rats, and these morphological alterations were normalized in
islets
from DEX(10) rats.
In parallel, the increased levels of proteins involved in β-cell proliferation such as Cd2 and Cdk4 observed in DEX
islets
were also normalized in DEX(10)
islets
.
CONCLUSION: These data strongly support the view that almost all the morphophysiological alterations induced by dexamethasone in the
endocrine pancreas
are reverted after discontinuation of the treatment.
[MeSH-major]
Dexamethasone / analogs & derivatives. Glucocorticoids / administration & dosage. Insulin / secretion.
Islets
of
Langerhans
/ drug effects
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[Copyright]
© 2010 The Authors. Journal compilation © 2010 Scandinavian Physiological Society.
(PMID = 20456283.001).
[ISSN]
1748-1716
[Journal-full-title]
Acta physiologica (Oxford, England)
[ISO-abbreviation]
Acta Physiol (Oxf)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Blood Glucose; 0 / Cell Cycle Proteins; 0 / Glucocorticoids; 0 / Insulin; 312-93-6 / dexamethasone 21-phosphate; 7S5I7G3JQL / Dexamethasone
82.
Ropero AB, Soriano S, Tudurí E, Marroquí L, Téllez N, Gassner B, Juan-Picó P, Montanya E, Quesada I, Kuhn M, Nadal A:
The atrial natriuretic peptide and guanylyl cyclase-A system modulates pancreatic beta-cell function.
Endocrinology
; 2010 Aug;151(8):3665-74
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Atrial natriuretic peptide (ANP) and its guanylyl cyclase-A (GC-A) receptor are being involved in metabolism, although their role in the
endocrine pancreas
is still greatly unknown.
GC-A activation by its natural ligand, ANP, rapidly blocked ATP-dependent potassium (K(ATP)) channel activity, increased glucose-elicited Ca(2+) signals, and enhanced GSIS in
islets
of
Langerhans
.
The effect in GSIS was inhibited in
islets
from GC-A knockout (KO) mice.
Pancreatic
islets
from GC-A KO mice responded to increasing glucose concentrations with enhanced insulin secretion compared with wild type (WT).
Remarkably,
islets
from GC-A KO mice were smaller, presented lower beta-cell mass and decreased insulin content.
However, glucose-induced Ca(2+) response was more vigorous in GC-A KO
islets
, and basal K(ATP) channel activity in GC-A KO beta-cells was greatly diminished compared with WT.
When protein levels of the two K(ATP) channel constitutive subunits sulfonylurea receptor 1 and Inward rectifier potassium channel 6.2 were measured, both were diminished in GC-A KO
islets
.
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KOMP Repository.
gene/protein/disease-specific - KOMP Repository
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.
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(PMID = 20555029.001).
[ISSN]
1945-7170
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Insulin; 0 / KATP Channels; 85637-73-6 / Atrial Natriuretic Factor; EC 4.6.1.2 / Receptors, Atrial Natriuretic Factor; EC 4.6.1.2 / atrial natriuretic factor receptor A; IY9XDZ35W2 / Glucose
83.
Dall'igna P, Cecchetto G, Bisogno G, Conte M, Chiesa PL, D'Angelo P, De Leonardis F, De Salvo G, Favini F, Ferrari A, TREP Group:
Pancreatic tumors in children and adolescents: the Italian TREP project experience.
Pediatr Blood Cancer
; 2010 May;54(5):675-80
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RESULTS:
Tumor
types were 4 pancreatoblastomas, 2 pancreatic carcinomas, 3 neoplasms of the
endocrine pancreas
, and 12 solid pseudopapillary tumors.
Three of the four patients with pancreatoblastoma had advanced disease at
diagnosis
and were given chemotherapy; at the time of this report, three patients were alive in first remission, while one died due to treatment toxicity.
Both the cases of pancreatic carcinoma had the acinar cell subtype and successfully underwent pancreaticoduodenectomy with complete
tumor
resection, remaining without evidence of disease at the time of this analysis.
The histological diagnoses of the three
endocrine
tumors were a malignant islet cell
tumor
, a gastrinoma, and a well-differentiated
tumor
.
All 12 patients with solid pseudopapillary tumors underwent complete
tumor
resection and were given no adjuvant treatment; 11 were alive in first remission, while one experienced a local and distant relapse 5 years after
diagnosis
.
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[CommentIn]
Pediatr Blood Cancer. 2010 May;54(5):659-60
[
20063425.001
]
(PMID = 19998473.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
84.
Rath MF, Bailey MJ, Kim JS, Ho AK, Gaildrat P, Coon SL, Møller M, Klein DC:
Developmental and diurnal dynamics of Pax4 expression in the mammalian pineal gland: nocturnal down-regulation is mediated by adrenergic-cyclic adenosine 3',5'-monophosphate signaling.
Endocrinology
; 2009 Feb;150(2):803-11
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Pax4 is a homeobox gene that is known to be involved in embryonic development of the
endocrine pancreas
.
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(PMID = 18818287.001).
[ISSN]
1945-7170
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
ENG
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / Paired Box Transcription Factors; 0 / Pax4 protein, rat; 0 / RNA, Messenger; 0 / Receptors, Adrenergic; E0399OZS9N / Cyclic AMP
[Other-IDs]
NLM/ PMC2646524
85.
Arciszewski MB:
Expression of neuronal nitric oxide synthase in the pancreas of the sheep.
Anat Histol Embryol
; 2007 Oct;36(5):375-81
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[Title]
Expression of neuronal nitric oxide synthase in the
pancreas of
the sheep.
In numerous mammals, nitric oxide (NO) influences the activity of the exocrine and
endocrine pancreas
.
In this study, immunocytochemistry was utilized to investigate the expression of neuronal nitric oxide synthase (nNOS) in the
pancreas of
sheep.
The presence of nNOS was confined to the intrapancreatic neurones (9.6 +/- 1.3%) as well as to nerve fibres of the
endocrine pancreas
and intrapancreatic ganglia. nNOS-immunoreactive (IR) neurones were round and oval in shape and predominantly (83.3 +/- 2.6%) belonged to the middle-size group (25-50 mum).
Numerous, fine
islets
supplying nNOS-IR nerve terminals were devoid of VIP, SP or NPY.
Comparison with other mammals indicated that nitrergic innervation of the ovine
pancreas
is species-determined and may be a reflection of the ruminants' digestion specificity.
The possible origin of nNOS-IR nerve fibres and functional significance of NO in the
pancreas of
sheep were discussed.
[MeSH-major]
Nitric Oxide Synthase / metabolism.
Pancreas
/ enzymology.
Pancreas
/ innervation
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(PMID = 17845229.001).
[ISSN]
0340-2096
[Journal-full-title]
Anatomia, histologia, embryologia
[ISO-abbreviation]
Anat Histol Embryol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / Neuropeptide Y; 33507-63-0 / Substance P; 37221-79-7 / Vasoactive Intestinal Peptide; EC 1.14.13.39 / Nitric Oxide Synthase
86.
Antoine M, Khitrik-Palchuk M, Saif MW:
Long-term survival in a patient with acinar cell carcinoma of pancreas. A case report and review of literature.
JOP
; 2007;8(6):783-9
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[Title]
Long-term survival in a patient with acinar cell carcinoma
of pancreas
. A case report and review of literature.
CONTEXT: Acinar cell carcinoma of the
pancreas
is a rare malignancy that may have acinar and
endocrine
differentiation.
However, treatment protocols for acinar cell carcinoma of the
pancreas
have not been standardized.
CASE REPORT: We describe a case of a 44-year-old woman presenting with low grade fever and mid-abdominal tenderness secondary to a pancreatic mass with acinar and
endocrine
differentiation metastatic to the liver.
The patient developed Clostridium difficile colitis and septic shock resulting in death 37 months after the
diagnosis
of acinar cell carcinoma of the
pancreas
.
CONCLUSION: This is a case of acinar cell carcinoma of the
pancreas
with an
endocrine
component, treated with multiple chemotherapeutic agents, in which the patient survived 37 months after
diagnosis
.
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(PMID = 17993731.001).
[ISSN]
1590-8577
[Journal-full-title]
JOP : Journal of the pancreas
[ISO-abbreviation]
JOP
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Italy
[Number-of-references]
28
87.
Gao N, White P, Doliba N, Golson ML, Matschinsky FM, Kaestner KH:
Foxa2 controls vesicle docking and insulin secretion in mature Beta cells.
Cell Metab
; 2007 Oct;6(4):267-79
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The winged-helix transcription factor Foxa2 regulates Pdx1 gene expression and fetal
endocrine pancreas
development.
We conclude that Foxa2 is required for both fetal
pancreas
development and the function of mature beta cells.
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(PMID = 17908556.001).
[ISSN]
1550-4131
[Journal-full-title]
Cell metabolism
[ISO-abbreviation]
Cell Metab.
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / R01-DK055342; United States / NIDDK NIH HHS / DK / U01-DK056947
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Foxa2 protein, mouse; 0 / Insulin; 135845-92-0 / Hepatocyte Nuclear Factor 3-beta
88.
Sordi V, Bertuzzi F, Piemonti L:
Diabetes mellitus: an opportunity for therapy with stem cells?
Regen Med
; 2008 May;3(3):377-97
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Restoration of damaged beta-cells by
endocrine pancreas
regeneration would be an ideal therapeutic option.
Although progress is encouraging, major gaps in our understanding of developmental biology of the
pancreas
and adult beta-cell dynamics remain to be bridged before a therapeutic application is made possible.
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(PMID = 18462060.001).
[ISSN]
1746-076X
[Journal-full-title]
Regenerative medicine
[ISO-abbreviation]
Regen Med
[Language]
eng
[Grant]
Italy / Telethon / / JT01Y01
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Blood Glucose; 0 / Insulin
[Number-of-references]
246
89.
Schreiber R, Levy J, Loewenthal N, Pinsk V, Hershkovitz E:
Decreased first phase insulin response in children with congenital insensitivity to pain with anhidrosis.
J Pediatr Endocrinol Metab
; 2005 Sep;18(9):873-7
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Nerve growth factor (NGF) and its receptor tyrosine kinase A (TrkA) participate in
endocrine pancreas
morphogenesis and insulin secretion in vitro.
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(PMID = 16279365.001).
[ISSN]
0334-018X
[Journal-full-title]
Journal of pediatric endocrinology & metabolism : JPEM
[ISO-abbreviation]
J. Pediatr. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Blood Glucose; 0 / Insulin; EC 2.7.10.1 / Receptor, trkA
90.
Tham E, Grandell U, Lindgren E, Toss G, Skogseid B, Nordenskjöld M:
Clinical testing for mutations in the MEN1 gene in Sweden: a report on 200 unrelated cases.
J Clin Endocrinol Metab
; 2007 Sep;92(9):3389-95
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CONTEXT: Multiple
endocrine
neoplasia
type 1 (MEN1) is a
tumor
syndrome of the parathyroid,
endocrine pancreas
, and anterior pituitary caused by mutations in the MEN1 gene on 11q13.
Individuals with at least one typical
endocrine
tumour
and at least one of the following:.
1) a first-degree relative with a major
endocrine tumor
;.
[MeSH-major]
DNA Mutational Analysis. Multiple
Endocrine
Neoplasia
Type 1 / genetics. Proto-Oncogene Proteins / genetics
NCI CPTC Antibody Characterization Program.
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(PMID = 17623761.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
91.
Anhê GF, Nogueira TC, Nicoletti-Carvalho JE, Lellis-Santos C, Barbosa HC, Cipolla-Neto J, Bosqueiro JR, Boschero AC, Bordin S:
Signal transducer and activator of transcription 3-regulated sarcoendoplasmic reticulum Ca2+-ATPase 2 expression by prolactin and glucocorticoids is involved in the adaptation of insulin secretory response during the peripartum period.
J Endocrinol
; 2007 Oct;195(1):17-27
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During pregnancy, the maternal
endocrine pancreas
undergoes, as a consequence of placental lactogens and prolactin (PRL) action, functional changes that are characterized by increased glucose-induced insulin secretion.
After delivery, the maternal
endocrine pancreas
rapidly returns to non-pregnant state, which is mainly attributed to the increased serum levels of glucocorticoids (GCs).
We have previously demonstrated that signal transducer and activator of transcription 3 (STAT3) is increased in
islets
treated with PRL.
In the present study, we show that STAT3 expression and serine phosphorylation are increased in pancreatic
islets
at the
end
of pregnancy (P19).
Insulin secretion from
islets
of P19 rats pre-incubated with thapsigargin and L3 rats showed a dramatic suppression of first phase of insulin release.
PRL effect is counteracted by DEX and might contribute to the adaptation of maternal
endocrine pancreas
during the peripartum period.
[MeSH-major]
Glucocorticoids / metabolism. Insulin / secretion.
Islets
of
Langerhans
/ secretion. Prolactin / metabolism. STAT3 Transcription Factor / metabolism. Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism
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(PMID = 17911393.001).
[ISSN]
0022-0795
[Journal-full-title]
The Journal of endocrinology
[ISO-abbreviation]
J. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Glucocorticoids; 0 / Insulin; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / STAT3 Transcription Factor; 0 / Stat3 protein, rat; 7S5I7G3JQL / Dexamethasone; 9002-62-4 / Prolactin; EC 3.6.3.8 / Atp2a2 protein, rat; EC 3.6.3.8 / Atp2a3 protein, rat; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases
92.
Kapasa M, Arhondakis S, Kossida S:
Phylogenetic and regulatory region analysis of Wnt5 genes reveals conservation of a regulatory module with putative implication in pancreas development.
Biol Direct
; 2010;5:49
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[Title]
Phylogenetic and regulatory region analysis of Wnt5 genes reveals conservation of a regulatory module with putative implication in
pancreas
development.
Interestingly, experimental data for some species indicated that only one of the two Wnt5 paralogs participates in the development of the
endocrine pancreas
.
Furthermore, an in silico regulatory region analysis of Wnt5 paralogs was conducted, limited to those species with insulin producing cells and
pancreas
, covering the evolutionary distance from agnatha to gnathostomata.
Moreover, within this latter region, a conserved module was detected to which a complex of transcription factors, known to be implicated in embryonic
pancreas
formation, bind.
CONCLUSIONS: Results and observations presented in this study, allow us to conclude that during evolution, the Wnt5 gene has been duplicated in early vertebrates, and that some paralogs conserved a module within their regulatory region, functionally related to embryonic development
of pancreas
.
Interestingly, our results allowed advancing a possible explanation on why the Wnt5 orthologs do not share the same function during
pancreas
development.
[MeSH-major]
Pancreas
/ embryology.
Pancreas
/ metabolism. Phylogeny. Wnt Proteins / genetics. Wnt Proteins / metabolism
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