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1. Lee M, Han SO, Ko KS, Koh JJ, Park JS, Yoon JW, Kim SW: Repression of GAD autoantigen expression in pancreas beta-Cells by delivery of antisense plasmid/PEG-g-PLL complex. Mol Ther; 2001 Oct;4(4):339-46
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  • We also transfected pRIP-AS-GAD/PEG-g-PLL complex into a GAD-producing mouse insulinoma (MIN6) cell line.
  • [MeSH-major] Autoantigens / biosynthesis. DNA, Antisense / therapeutic use. Gene Expression Regulation, Enzymologic. Glutamate Decarboxylase / biosynthesis. Islets of Langerhans / metabolism. Polyethylene Glycols / metabolism. Polylysine / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Drug Carriers / metabolism. Injections, Intravenous. Insulinoma / genetics. Insulinoma / metabolism. Male. Mice. Organ Specificity. Plasmids / administration & dosage. Plasmids / genetics. Plasmids / therapeutic use. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Transfection / methods. Tumor Cells, Cultured. beta-Galactosidase / genetics. beta-Galactosidase / metabolism

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  • (PMID = 11592837.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK51689
  • [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 / Autoantigens; 0 / DNA, Antisense; 0 / Drug Carriers; 0 / RNA, Messenger; 25104-18-1 / Polylysine; 30IQX730WE / Polyethylene Glycols; EC 3.2.1.23 / beta-Galactosidase; EC 4.1.1.15 / Glutamate Decarboxylase
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2. Wicki A, Wild D, Storch D, Seemayer C, Gotthardt M, Behe M, Kneifel S, Mihatsch MJ, Reubi JC, Mäcke HR, Christofori G: [Lys40(Ahx-DTPA-111In)NH2]-Exendin-4 is a highly efficient radiotherapeutic for glucagon-like peptide-1 receptor-targeted therapy for insulinoma. Clin Cancer Res; 2007 Jun 15;13(12):3696-705
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  • [Title] [Lys40(Ahx-DTPA-111In)NH2]-Exendin-4 is a highly efficient radiotherapeutic for glucagon-like peptide-1 receptor-targeted therapy for insulinoma.
  • PURPOSE: Although metabolic changes make diagnosis of insulinoma relatively easy, surgical removal is hampered by difficulties in locating it, and there is no efficient treatment for malignant insulinoma.
  • We have previously shown that the high density of glucagon-like peptide-1 receptors (GLP-1R) in human insulinoma cells provides an attractive target for molecular imaging and internal radiotherapy.
  • In this study, we investigated the therapeutic potential of [Lys(40)(Ahx-DTPA-(111)In)NH(2)]-Exendin-4, an (111)In-labeled agonist of GLP-1, in a transgenic mouse model of human insulinoma.
  • EXPERIMENTAL DESIGN: [Lys(40)(Ahx-DTPA-(111)In)NH(2)]-Exendin-4 was assessed in the Rip1Tag2 mouse model of pancreatic beta-cell carcinogenesis, which exhibits a GLP-1R expression comparable with human insulinoma.
  • Tumor uptake and response, the mechanism of action of the radiopeptide, and therapy toxicity were investigated.
  • RESULTS: Tumor uptake was >200% injected activity per gram, with a dose deposition of 3 Gy/MBq at 40 pmol [Lys(40)(Ahx-DTPA-(111)In)NH(2)]-Exendin-4.
  • Other GLP-1R-positive organs showed > or =30 times lower dose deposition.
  • The therapeutic effect was due to increased tumor cell apoptosis and necrosis and decreased proliferation.
  • CONCLUSIONS: The results suggest that [Lys(40)(Ahx-DTPA-(111)In)NH(2)]-Exendin-4 is a promising radiopeptide capable of selectively targeting insulinoma.
  • Furthermore, Auger-emitting radiopharmaceuticals such as (111)In are able to produce a marked therapeutic effect if a high tumor uptake is achieved.
  • [MeSH-major] Indium Radioisotopes / therapeutic use. Insulinoma / radionuclide imaging. Organometallic Compounds / therapeutic use. Pancreatic Neoplasms / radionuclide imaging. Peptides / therapeutic use. Radiopharmaceuticals / therapeutic use. Receptors, Glucagon / metabolism
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Female. Glucagon-Like Peptide-1 Receptor. Male. Mice. Mice, Transgenic. Pentetic Acid / pharmacokinetics. Pentetic Acid / therapeutic use. Tissue Distribution

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  • (PMID = 17575235.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / (Lys(40)(Ahx-DTPA-111In)NH2)exendin-14; 0 / GLP1R protein, human; 0 / Glp1r protein, mouse; 0 / Glucagon-Like Peptide-1 Receptor; 0 / Indium Radioisotopes; 0 / Organometallic Compounds; 0 / Peptides; 0 / Radiopharmaceuticals; 0 / Receptors, Glucagon; 7A314HQM0I / Pentetic Acid
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3. Yang JY, Walicki J, Abderrahmani A, Cornu M, Waeber G, Thorens B, Widmann C: Expression of an uncleavable N-terminal RasGAP fragment in insulin-secreting cells increases their resistance toward apoptotic stimuli without affecting their glucose-induced insulin secretion. J Biol Chem; 2005 Sep 23;280(38):32835-42
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  • Apoptosis of pancreatic beta cells is implicated in the onset of type 1 and type 2 diabetes.
  • Consequently, strategies aimed at increasing the resistance of beta cells toward apoptosis could be beneficial in the treatment of diabetes.
  • Here we demonstrate that an uncleavable form of fragment N activates Akt, represses NF-kappaB activity, and protects the conditionally immortalized pancreatic insulinoma betaTC-tet cell line against various insults, including exposure to genotoxins, trophic support withdrawal, and incubation with inflammatory cytokines.
  • The pathways regulated by fragment N are therefore promising targets for antidiabetogenic therapy.
  • [MeSH-minor] Animals. Caspase 3. Caspases / metabolism. Cell Line. Cisplatin / pharmacology. Cross-Linking Reagents / pharmacology. Cytokines / metabolism. Dose-Response Relationship, Drug. Humans. Immunohistochemistry. Inflammation. Insulinoma / metabolism. Lentivirus / genetics. Mice. Microscopy, Fluorescence. NF-kappa B / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Plasmids / metabolism. Protein Binding. Protein Structure, Tertiary. Rats. Rats, Wistar. Time Factors

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  • (PMID = 16046410.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cross-Linking Reagents; 0 / Cytokines; 0 / Insulin; 0 / NF-kappa B; 0 / ras GTPase-Activating Proteins; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Casp3 protein, rat; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; IY9XDZ35W2 / Glucose; Q20Q21Q62J / Cisplatin
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4. Mziaut H, Kersting S, Knoch KP, Fan WH, Trajkovski M, Erdmann K, Bergert H, Ehehalt F, Saeger HD, Solimena M: ICA512 signaling enhances pancreatic beta-cell proliferation by regulating cyclins D through STATs. Proc Natl Acad Sci U S A; 2008 Jan 15;105(2):674-9
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  • We now show that knockdown of ICA512 decreases cyclin D1 levels and proliferation of insulinoma INS-1 cells, whereas beta-cell regeneration is reduced in partially pancreatectomized ICA512-/- mice.
  • These results identify ICA512 as a regulator of cyclins D and beta-cell proliferation through STATs and may have implication for diabetes therapy.
  • [MeSH-minor] Animals. Cell Proliferation. Cyclin D. Cyclin D2. Diabetes Mellitus / drug therapy. Diabetes Mellitus / metabolism. Humans. Insulin / metabolism. Models, Biological. Phosphorylation. Rats. Regeneration. Signal Transduction


5. Bara H, Thulé PM, Sambanis A: A cell-based approach for diabetes treatment using engineered non-beta cells. J Diabetes Sci Technol; 2009 May 01;3(3):555-61
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  • [Title] A cell-based approach for diabetes treatment using engineered non-beta cells.
  • To overcome the limitations of tissue availability and recipient immunosuppression, encapsulation of nonautologous cells and use of potentially autologous nonislet cells, the latter engineered for insulin secretion, are being pursued.
  • This article reports on recent findings with the implantation of tissue constructs containing enteroendocrine cells stably expressing recombinant insulin in diabetic mice.
  • METHODS: Mouse GLUTag-INS cells engineered to secrete human insulin were developed and incorporated in tissue constructs as reported previously.
  • Constructs were implanted intraperitoneally in diabetic mice, and blood glucose levels, animal weights, and plasma insulin levels were measured at various time points.
  • RESULTS: GLUTag-INS-containing tissue constructs secreted insulin preimplantation and postexplantation, and human insulin was detected in the plasma of diabetic mice.
  • CONCLUSIONS: A variety of cell types and of encapsulation methods to enhance immune acceptance of insulin-secreting grafts are being pursued.
  • [MeSH-major] Bioengineering. Cell- and Tissue-Based Therapy / methods. Diabetes Mellitus, Experimental / therapy. Enteroendocrine Cells / metabolism. Enteroendocrine Cells / transplantation. Insulin / metabolism
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Transplantation. Disease Models, Animal. Humans. Insulinoma / pathology. Mice. Mice, Inbred C57BL. Pancreatic Neoplasms / pathology. Streptozocin

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  • [Copyright] 2009 Diabetes Technology Society.
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  • (PMID = 20144295.001).
  • [ISSN] 1932-2968
  • [Journal-full-title] Journal of diabetes science and technology
  • [ISO-abbreviation] J Diabetes Sci Technol
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / R01DK076801
  • [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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 5W494URQ81 / Streptozocin
  • [Other-IDs] NLM/ PMC2769879
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6. Mancuso MR, Davis R, Norberg SM, O'Brien S, Sennino B, Nakahara T, Yao VJ, Inai T, Brooks P, Freimark B, Shalinsky DR, Hu-Lowe DD, McDonald DM: Rapid vascular regrowth in tumors after reversal of VEGF inhibition. J Clin Invest; 2006 Oct;116(10):2610-21
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  • Inhibitors of VEGF signaling can block angiogenesis and reduce tumor vascularity, but little is known about the reversibility of these changes after treatment ends.
  • One day after drug withdrawal, endothelial sprouts grew into empty sleeves of basement membrane.
  • Importantly, the regrown vasculature regressed as much during a second treatment as it did in the first.
  • Inhibition of MMPs or targeting of type IV collagen cryptic sites by antibody HUIV26 did not eliminate the sleeves or slow revascularization.
  • These results suggest that empty sleeves of basement membrane and accompanying pericytes provide a scaffold for rapid revascularization of tumors after removal of anti-VEGF therapy and highlight their importance as potential targets in cancer therapy.

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  • (PMID = 17016557.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL-24136; United States / NHLBI NIH HHS / HL / P01 HL024136; United States / NCI NIH HHS / CA / R01 CA082923; United States / NCI NIH HHS / CA / P50-CA90270; United States / NCI NIH HHS / CA / P50 CA090270; United States / NHLBI NIH HHS / HL / R01 HL059157; United States / NCI NIH HHS / CA / CA082923; United States / NHLBI NIH HHS / HL / HL-59157
  • [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 / Actins; 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antigens, CD31; 0 / Collagen Type IV; 0 / Imidazoles; 0 / Indazoles; 0 / Matrix Metalloproteinase Inhibitors; 0 / Organic Chemicals; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 10T6626FRK / prinomastat; C9LVQ0YUXG / axitinib; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  • [Other-IDs] NLM/ PMC1578604
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7. Djokovic D, Trindade A, Gigante J, Badenes M, Silva L, Liu R, Li X, Gong M, Krasnoperov V, Gill PS, Duarte A: Combination of Dll4/Notch and Ephrin-B2/EphB4 targeted therapy is highly effective in disrupting tumor angiogenesis. BMC Cancer; 2010 Nov 23;10:641
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  • [Title] Combination of Dll4/Notch and Ephrin-B2/EphB4 targeted therapy is highly effective in disrupting tumor angiogenesis.
  • This study evaluates the efficacy of the inhibition of both signaling pathways, alone and in combination, in reducing the growth of an autochthonous mouse tumor and assesses potential adverse effects.
  • RESULTS: Dll4 allele deletion or soluble Dll4 treatment resulted in increased tumor vessel density, reduced mural cell recruitment and vessel perfusion which resulted in reduced tumor size.
  • Induced endothelial specific Dll4 loss-of-function caused hepatic vascular alterations, which were prevented by concomitant sEphB4-Alb treatment.

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  • (PMID = 21092311.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 079218-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / DLL4 protein, mouse; 0 / Ephrin-B2; 0 / Intracellular Signaling Peptides and Proteins; 0 / Membrane Proteins; 0 / Receptors, Notch; 0 / Recombinant Fusion Proteins; EC 2.7.1.- / Ephb4 protein, mouse; EC 2.7.10.1 / Receptor, EphB4
  • [Other-IDs] NLM/ PMC3001720
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8. Bergmann F, Breinig M, Höpfner M, Rieker RJ, Fischer L, Köhler C, Esposito I, Kleeff J, Herpel E, Ehemann V, Friess H, Schirmacher P, Kern MA: Expression pattern and functional relevance of epidermal growth factor receptor and cyclooxygenase-2: novel chemotherapeutic targets in pancreatic endocrine tumors? Am J Gastroenterol; 2009 Jan;104(1):171-81
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although many well-differentiated endocrine carcinomas show rather low rates of tumor growth, more than two-thirds of pancreatic endocrine carcinomas display distant metastases at the time of diagnosis.
  • As the currently applied therapies beyond surgery only achieve partial or complete response rates of approximately 15%, additional chemotherapeutic targets are needed, especially in the therapy of inoperable and progressive pancreatic endocrine carcinomas.
  • Functional tests were performed using the human pancreas carcinoid cell line BON and the mouse insulinoma cell line beta-TC-3.
  • The treatment of the human pancreas carcinoid cell line BON and the mouse insulinoma cell line beta-TC-3 with EGFR and COX-2 inhibitors (monotherapy and combined therapy) resulted in a significant, dose-dependent reduction of cell viability coupled with increased apoptosis.
  • [MeSH-major] Cyclooxygenase 2 / metabolism. Pancreatic Neoplasms / metabolism. Pyrazoles / therapeutic use. Receptor, Epidermal Growth Factor / metabolism. Sulfonamides / therapeutic use. Tyrphostins / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Apoptosis / drug effects. Blotting, Western. Carcinoid Tumor / metabolism. Celecoxib. Cell Line, Tumor. Cell Survival / drug effects. Cyclooxygenase 2 Inhibitors / therapeutic use. Dose-Response Relationship, Drug. Female. Humans. Insulinoma / metabolism. Male. Mice. Mice, Transgenic. Middle Aged. Quinazolines. Tumor Cells, Cultured. Young Adult

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  • (PMID = 19098866.001).
  • [ISSN] 1572-0241
  • [Journal-full-title] The American journal of gastroenterology
  • [ISO-abbreviation] Am. J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cyclooxygenase 2 Inhibitors; 0 / Pyrazoles; 0 / Quinazolines; 0 / Sulfonamides; 0 / Tyrphostins; 170449-18-0 / tyrphostin AG 1478; EC 1.14.99.1 / Cyclooxygenase 2; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; JCX84Q7J1L / Celecoxib
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9. Jeong JH, Lee M, Kim WJ, Yockman JW, Park TG, Kim YH, Kim SW: Anti-GAD antibody targeted non-viral gene delivery to islet beta cells. J Control Release; 2005 Oct 20;107(3):562-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The PEI-PEG-Fab' showed about 10-fold higher transfection efficiency (relative luciferase activity) than PEI-PEG in GAD-expressing mouse insulinoma cells (MIN6), however the transfection efficiency of PEI-PEG-Fab' reduced to that of PEI-PEG in GAD negative cells (293) and in the presence of competitive free Fab'.
  • Considering the neutral surface charge of its complexes with DNA, and selectivity toward the islet cells expressing a specific antigen, the PEI-PEG-Fab' conjugate could be thought as a potential candidate of the systemic gene therapy for the treatment of type I diabetes.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / immunology. Drug Delivery Systems. Genetic Therapy / methods. Glutamate Decarboxylase / immunology. Insulin-Secreting Cells / drug effects. Insulin-Secreting Cells / immunology
  • [MeSH-minor] Animals. Cell Survival / drug effects. Electrophoresis, Agar Gel. Immunoglobulin Fab Fragments / genetics. Mice. Microscopy, Confocal. Polyethylene Glycols. Polyethyleneimine. Transfection

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  • (PMID = 16139384.001).
  • [ISSN] 0168-3659
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [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] Netherlands
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Fab Fragments; 30IQX730WE / Polyethylene Glycols; 9002-98-6 / Polyethyleneimine; EC 4.1.1.15 / Glutamate Decarboxylase
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10. Størling J, Allaman-Pillet N, Karlsen AE, Billestrup N, Bonny C, Mandrup-Poulsen T: Antitumorigenic effect of proteasome inhibitors on insulinoma cells. Endocrinology; 2005 Apr;146(4):1718-26
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  • [Title] Antitumorigenic effect of proteasome inhibitors on insulinoma cells.
  • Malignant insulinoma is a critical cancer form with a poor prognosis.
  • Because cure by surgery is infrequent, effective chemotherapy is in demand.
  • Induction of cell death in tumor cells by proteasome inhibitors is emerging as a potential strategy in cancer therapy.
  • Here we investigated whether inhibition of the proteasome has an antitumorigenic potential in insulinoma cells.
  • Exposure of mouse betaTC3 insulinoma cells to the proteasome inhibitor N-Acetyl-Leu-Leu-Nle-CHO (ALLN) reduced cell viability, activated caspase-3, induced apoptosis, and suppressed insulin release.
  • Treatment with ALLN also resulted in phosphorylation of c-jun N-terminal kinase (JNK) and an increase in in vitro phosphorylation of c-jun.
  • In insulinoma cells with impaired JNK signaling, ALLN-induced apoptosis was significantly suppressed.
  • Our findings demonstrate that proteasome inhibitors possess antitumorigenic and antiinsulinogenic effects on insulinoma cells.
  • [MeSH-major] Acetylcysteine / analogs & derivatives. Antineoplastic Agents / pharmacology. Cysteine Proteinase Inhibitors / pharmacology. Insulinoma / drug therapy. Pancreatic Neoplasms / drug therapy. Proteasome Inhibitors
  • [MeSH-minor] Adaptor Proteins, Signal Transducing / antagonists & inhibitors. Animals. Apoptosis / drug effects. Binding Sites. Cell Line, Tumor. JNK Mitogen-Activated Protein Kinases / metabolism. Leupeptins / pharmacology. Mice. Rats. Signal Transduction / drug effects. Tumor Suppressor Protein p53 / metabolism

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  • (PMID = 15618349.001).
  • [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 / Adaptor Proteins, Signal Transducing; 0 / Antineoplastic Agents; 0 / Cysteine Proteinase Inhibitors; 0 / Leupeptins; 0 / Mapk8ip protein, mouse; 0 / Proteasome Inhibitors; 0 / Tumor Suppressor Protein p53; 110044-82-1 / acetylleucyl-leucyl-norleucinal; 133343-34-7 / lactacystin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; WYQ7N0BPYC / Acetylcysteine
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11. Huang L, Yan M, Kirschke CP: Over-expression of ZnT7 increases insulin synthesis and secretion in pancreatic beta-cells by promoting insulin gene transcription. Exp Cell Res; 2010 Oct 1;316(16):2630-43
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  • In this study, we demonstrated that zinc transporter 7 (ZnT7, Slc30a7) was co-expressed with insulin in the islet of Langerhans in the mouse pancreas.
  • In RIN5mF cells (rat insulinoma cells), ZnT7 was found mainly residing in the perinuclear region of the cell, which is consistent with its Golgi apparatus localization.
  • [MeSH-major] Cation Transport Proteins / metabolism. Glucose / pharmacology. Insulin / genetics. Insulin / secretion. Insulin-Secreting Cells / metabolism. Transcription, Genetic / drug effects
  • [MeSH-minor] Animals. Blotting, Western. Cells, Cultured. Electrophoretic Mobility Shift Assay. Fluorescent Antibody Technique. Immunoprecipitation. Insulinoma / drug therapy. Insulinoma / metabolism. Insulinoma / pathology. Islets of Langerhans / cytology. Islets of Langerhans / metabolism. Male. Mice. Mice, Inbred C57BL. RNA, Messenger / genetics. Rats. Reverse Transcriptase Polymerase Chain Reaction

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  • [Copyright] Published by Elsevier Inc.
  • (PMID = 20599947.001).
  • [ISSN] 1090-2422
  • [Journal-full-title] Experimental cell research
  • [ISO-abbreviation] Exp. Cell Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cation Transport Proteins; 0 / Insulin; 0 / RNA, Messenger; 0 / ZnT7 protein, mouse; IY9XDZ35W2 / Glucose
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12. Luo LG, Jackson I: Thyrotropin releasing hormone (TRH) may preserve pancreatic islet cell function: potential role in the treatment of diabetes mellitus. Acta Biomed; 2007;78 Suppl 1:216-21
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thyrotropin releasing hormone (TRH) may preserve pancreatic islet cell function: potential role in the treatment of diabetes mellitus.
  • The significance of this association is emphasised by the report that the TRH knock-out (KO) mouse is hyperglycemic.
  • These studies point to a potential therapeutic role for TRH in the treatment of DM in man.
  • [MeSH-major] Diabetes Mellitus / drug therapy. Islets of Langerhans / drug effects. Thyrotropin-Releasing Hormone / physiology
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Line, Tumor / metabolism. Diabetes Mellitus, Experimental / drug therapy. Drug Evaluation, Preclinical. Forecasting. Gene Expression Regulation. Homeostasis. Humans. Hyperglycemia / drug therapy. Insulin / secretion. Insulinoma / metabolism. Insulinoma / pathology. Mice. Mice, Knockout. Pancreatic Neoplasms / metabolism. Pancreatic Neoplasms / pathology. Rabbits. Rats. Stem Cells / drug effects. Streptozocin

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  • (PMID = 17465334.001).
  • [ISSN] 0392-4203
  • [Journal-full-title] Acta bio-medica : Atenei Parmensis
  • [ISO-abbreviation] Acta Biomed
  • [Language] eng
  • [Publication-type] Lectures
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 5W494URQ81 / Streptozocin; 5Y5F15120W / Thyrotropin-Releasing Hormone
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13. Yamada C, Nagashima K, Takahashi A, Ueno H, Kawasaki Y, Yamada Y, Seino Y, Inagaki N: Gatifloxacin acutely stimulates insulin secretion and chronically suppresses insulin biosynthesis. Eur J Pharmacol; 2006 Dec 28;553(1-3):67-72
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  • Gatifloxacin-induced hypoglycemia is associated with concomitant use of sulfonylureas, and usually occurs immediately after administration of the drug.
  • We find that gatifloxacin acutely stimulates insulin secretion from mouse pancreatic islets and that glibenclamide has additive effects on gatifloxacin-induced insulin secretion.
  • We also demonstrate that chronic gatifloxacin treatment decreases islet insulin content by inhibiting insulin biosynthesis, which process may be associated with gatifloxacin-induced hyperglycemia.
  • Because the risk of potentially life-threatening dysglycemia is increased during gatifloxacin therapy, these findings have important implications for clinical practice.
  • [MeSH-minor] Animals. Blood Glucose / metabolism. Cell Line, Tumor. Cell Separation. Glyburide / pharmacology. Hypoglycemic Agents / pharmacology. In Vitro Techniques. Insulinoma / metabolism. Islets of Langerhans / drug effects. Islets of Langerhans / secretion. Male. Mice. Mice, Inbred C57BL. Pancreatic Neoplasms / metabolism. Quinolones / pharmacology. RNA, Messenger / biosynthesis

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  • (PMID = 17070519.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Blood Glucose; 0 / Fluoroquinolones; 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Insulin Antagonists; 0 / Quinolones; 0 / RNA, Messenger; L4618BD7KJ / gatifloxacin; SX6K58TVWC / Glyburide
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14. Codd EE, Baker J, Brandt MR, Bryant S, Cai C, Carson JR, Chevalier KM, Colburn RW, Coogan TP, Dax SL, Decorte B, Kemmerer M, Legrand EK, Lenhard JM, Leone AM, Lin L, Mabus JR, McDonnell ME, McMillian MK, McNally JJ, Stone DJ Jr, Wang CY, Zhang SP, Flores CM: Diabetogenic effect of a series of tricyclic delta opioid agonists structurally related to cyproheptadine. Toxicol Sci; 2010 Oct;117(2):493-504
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  • A review of the literature on the antiserotonergic and antihistaminergic drug cyproheptadine (CPH) and its metabolites revealed shared structural features as well as similar hyperglycemic effects to the present series of DOR agonists.
  • Furthermore, the RINm5F cell insulin results correlated with the diabetogenic effect of the compounds in a 5-day mouse study.
  • [MeSH-major] Cyproheptadine / toxicity. Hyperglycemia / chemically induced. Insulin-Secreting Cells / drug effects. Narcotic Antagonists / toxicity. Pancreas / drug effects. Serotonin Antagonists / toxicity
  • [MeSH-minor] Animals. Blood Glucose / analysis. Blood Glucose / drug effects. Cell Enlargement / drug effects. Cell Line, Tumor. Diabetes Mellitus, Type 1 / metabolism. Dogs. Epiphyses / abnormalities. Epiphyses / metabolism. Female. High-Throughput Screening Assays. Insulin / blood. Insulinoma / drug therapy. Insulinoma / metabolism. Male. Mice. Osteochondrodysplasias / metabolism. Rats. Rats, Sprague-Dawley. Vacuoles / drug effects. Vacuoles / ultrastructure

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  • (PMID = 20616206.001).
  • [ISSN] 1096-0929
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Narcotic Antagonists; 0 / Serotonin Antagonists; 2YHB6175DO / Cyproheptadine; Wolcott-Rallison syndrome
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15. Nakamura A, Terauchi Y, Ohyama S, Kubota J, Shimazaki H, Nambu T, Takamoto I, Kubota N, Eiki J, Yoshioka N, Kadowaki T, Koike T: Impact of small-molecule glucokinase activator on glucose metabolism and beta-cell mass. Endocrinology; 2009 Mar;150(3):1147-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We analyzed four mouse groups: wild-type mice and beta-cell-specific haploinsufficiency of glucokinase gene (Gck(+/-)) mice on a high-fat (HF) diet.
  • Rodent insulinoma cells and isolated islets were used to evaluate beta-cell proliferation by GKA.
  • Glucose tolerance was improved shortly after the GKA treatment in both genotypes of mice. beta-Cell mass increased in wild-type mice compared with Gck(+/-) mice, but a further increase was not observed after the administration of GKA in both genotypes.
  • Interestingly, GKA was able to up-regulate insulin receptor substrate-2 (Irs-2) expression in insulinoma cells and isolated islets.
  • The administration of GKA increased 5-bromo-2-deoxyuridine (BrdU) incorporation in insulinoma cells, and 3 d administration of GKA markedly increased BrdU incorporation in mice treated with GKA in both genotypes, compared with those without GKA.
  • This apparent discrepancy can be explained by a chronic reduction in ambient blood glucose levels by GKA treatment.
  • [MeSH-minor] Animals. Body Weight / drug effects. Bromodeoxyuridine / pharmacokinetics. Cells, Cultured. Diet, Atherogenic. Dietary Fats / pharmacology. Drug Evaluation, Preclinical. Enzyme Activation / drug effects. Enzyme Activation / physiology. Glucose Intolerance / drug therapy. Insulin / secretion. Insulin Receptor Substrate Proteins / genetics. Insulin Receptor Substrate Proteins / metabolism. Mice. Mice, Transgenic. Organ Size / drug effects

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  • (PMID = 19008318.001).
  • [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 / Dietary Fats; 0 / Hypoglycemic Agents; 0 / Insulin; 0 / Insulin Receptor Substrate Proteins; 0 / Irs2 protein, rat; EC 2.7.1.2 / Glucokinase; G34N38R2N1 / Bromodeoxyuridine; IY9XDZ35W2 / Glucose
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16. Abe M, Toyohara T, Ishii A, Suzuki T, Noguchi N, Akiyama Y, Shiwaku HO, Nakagomi-Hagihara R, Zheng G, Shibata E, Souma T, Shindo T, Shima H, Takeuchi Y, Mishima E, Tanemoto M, Terasaki T, Onogawa T, Unno M, Ito S, Takasawa S, Abe T: The HMG-CoA reductase inhibitor pravastatin stimulates insulin secretion through organic anion transporter polypeptides. Drug Metab Pharmacokinet; 2010;25(3):274-82
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  • Rat oatp1/slco1a1, oatp2/slco1a4 and oatp3/slco1a5 were expressed in the pancreas, and rat oatp3/slco1a5 was also detected in rat insulinoma cell line INS-1e.
  • [MeSH-minor] Adiponectin / blood. Animals. Biological Transport / drug effects. Cell Line, Tumor. Diabetes Mellitus / drug therapy. Hydroxymethylglutaryl CoA Reductases. Immunohistochemistry. Male. Mice. Mice, Inbred Strains. Models, Animal. Pancreas / cytology. Pancreas / drug effects. Rats. Rifampin / pharmacology. Sulfobromophthalein / pharmacology

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  • (PMID = 20610886.001).
  • [ISSN] 1880-0920
  • [Journal-full-title] Drug metabolism and pharmacokinetics
  • [ISO-abbreviation] Drug Metab. Pharmacokinet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Adiponectin; 0 / Adipoq protein, mouse; 0 / Insulin; 0 / Organic Anion Transporters, Sodium-Independent; 0C2P5QKL36 / Sulfobromophthalein; EC 1.1.1.- / Hydroxymethylglutaryl CoA Reductases; KXO2KT9N0G / Pravastatin; VJT6J7R4TR / Rifampin
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17. Priel T, Aricha-Tamir B, Sekler I: Clioquinol attenuates zinc-dependent beta-cell death and the onset of insulitis and hyperglycemia associated with experimental type I diabetes in mice. Eur J Pharmacol; 2007 Jun 22;565(1-3):232-9
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  • [Title] Clioquinol attenuates zinc-dependent beta-cell death and the onset of insulitis and hyperglycemia associated with experimental type I diabetes in mice.
  • We further assessed the ability of clioquinol to protect the islets in an experimental model of type I diabetes.
  • Our results indicate that endogenous mechanisms for lowering [Zn]i are deficient in the insulinoma cell line, MIN6, and that permeation of Zn2+ triggered cell death.
  • Taken together, our results point to the potential utility of in vivo zinc chelation as a therapeutic strategy for treatment of idiopathic type I diabetes.
  • [MeSH-major] Chelating Agents / therapeutic use. Clioquinol / therapeutic use. Diabetes Mellitus, Type 1 / drug therapy. Hyperglycemia / drug therapy. Insulin-Secreting Cells / drug effects. Zinc / toxicity
  • [MeSH-minor] Animals. Cation Transport Proteins / analysis. Cell Death / drug effects. Cell Line, Tumor. Male. Mice. Mice, Inbred ICR. Sodium / metabolism. Streptozocin

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  • (PMID = 17434477.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cation Transport Proteins; 0 / Chelating Agents; 0 / Slc30a1 protein, mouse; 5W494URQ81 / Streptozocin; 7BHQ856EJ5 / Clioquinol; 9NEZ333N27 / Sodium; J41CSQ7QDS / Zinc
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18. Lu YR, Yuan Y, Wang XJ, Wei LL, Chen YN, Cong C, Li SF, Long D, Tan WD, Mao YQ, Zhang J, Li YP, Cheng JQ: The growth inhibitory effect of mesenchymal stem cells on tumor cells in vitro and in vivo. Cancer Biol Ther; 2008 Feb;7(2):245-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • MSCs were isolated from mouse bone marrow and cocultured with murine hepatoma H22, lymphoma (YAC-1 and EL-4) and rat insulinoma INS-1 cell lines.
  • [MeSH-major] Cell Proliferation / drug effects. Mesenchymal Stromal Cells / physiology. Neoplasms / pathology
  • [MeSH-minor] Animals. Apoptosis. Cell Cycle. Cell Line, Tumor. Cell Survival. Coculture Techniques. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Rats. Spleen / cytology. Spleen / immunology. Spleen / metabolism. Tetrazolium Salts / metabolism. Time Factors

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  • [CommentIn] Cancer Biol Ther. 2008 Feb;7(2):252-4 [18347432.001]
  • (PMID = 18059192.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tetrazolium Salts
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19. Kimple ME, Joseph JW, Bailey CL, Fueger PT, Hendry IA, Newgard CB, Casey PJ: Galphaz negatively regulates insulin secretion and glucose clearance. J Biol Chem; 2008 Feb 22;283(8):4560-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Clues to one potential function recently emerged with the finding that activation of Galphaz inhibits glucose-stimulated insulin secretion in an insulinoma cell line (Kimple, M.
  • To extend this study in vivo, a Galphaz knock-out mouse model was utilized to determine whether Galphaz function plays a role in the inhibition of insulin secretion.
  • No differences were discovered in the gross morphology of the pancreatic islets or in the islet DNA, protein, or insulin content between Galphaz-null and wild-type mice.
  • There was also no difference between the insulin sensitivity of Galphaz-null mice and wild-type controls, as measured by insulin tolerance tests.
  • Galphaz-null mice did, however, display increased plasma insulin concentrations and a corresponding increase in glucose clearance following intraperitoneal and oral glucose challenge as compared with wild-type controls.
  • The increased plasma insulin observed in Galphaz-null mice is most likely a direct result of enhanced insulin secretion, since pancreatic islets isolated from Galphaz-null mice exhibited significantly higher glucose-stimulated insulin secretion than those of wild-type mice.
  • These findings indicate that Galphaz may be a potential new target for therapeutics aimed at ameliorating beta-cell dysfunction in Type 2 diabetes.

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  • (PMID = 18096703.001).
  • [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 / GM55717; United States / NIDDK NIH HHS / DK / K01 DK080845; United States / NIDDK NIH HHS / DK / F32 DK067799; United States / NIDDK NIH HHS / DK / DK67799; United States / NIDDK NIH HHS / DK / DK42583
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / GTP-Binding Protein alpha Subunits; 0 / Insulin; 0 / Sweetening Agents; E0399OZS9N / Cyclic AMP; EC 4.6.1.1 / Adenylyl Cyclases; IY9XDZ35W2 / Glucose
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20. Harrison LC, Honeyman MC, Steele CE, Stone NL, Sarugeri E, Bonifacio E, Couper JJ, Colman PG: Pancreatic beta-cell function and immune responses to insulin after administration of intranasal insulin to humans at risk for type 1 diabetes. Diabetes Care; 2004 Oct;27(10):2348-55
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic beta-cell function and immune responses to insulin after administration of intranasal insulin to humans at risk for type 1 diabetes.
  • OBJECTIVE: Mucosal administration of insulin retards development of autoimmune diabetes in the nonobese diabetic mouse model.
  • We conducted a double-blind crossover study in humans at risk for type 1 diabetes to determine if intranasal insulin was safe, in particular did not accelerate beta-cell destruction, and could induce immune effects consistent with mucosal tolerance.
  • RESEARCH DESIGN AND METHODS: A total of 38 individuals, median age 10.8 years, with antibodies to one or more pancreatic islet antigens (insulin, GAD65, or tyrosine phosphatase-like insulinoma antigen 2) were randomized to treatment with intranasal insulin (1.6 mg) or a carrier solution, daily for 10 days and then 2 days a week for 6 months, before crossover.
  • Diabetes developed in 12 participants with negligible beta-cell function at entry after a median of 1.1 year.
  • CONCLUSIONS: Results from this pilot study suggest that intranasal insulin does not accelerate loss of beta-cell function in individuals at risk for type 1 diabetes and induces immune changes consistent with mucosal tolerance to insulin.
  • [MeSH-major] Diabetes Mellitus, Type 1 / prevention & control. Insulin / administration & dosage. Insulin Antibodies / analysis. Islets of Langerhans / drug effects. Prediabetic State / drug therapy
  • [MeSH-minor] Administration, Intranasal. Adolescent. Adult. Autoimmune Diseases / prevention & control. Blood Glucose / analysis. Blood Glucose / drug effects. Child. Cross-Over Studies. Dose-Response Relationship, Drug. Double-Blind Method. Drug Administration Schedule. Female. Follow-Up Studies. Glucose Tolerance Test. Humans. Male. Nasal Mucosa / drug effects. Reference Values. Risk Assessment. Severity of Illness Index. Treatment Outcome

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  • [Copyright] Copyright 2004 American Diabetes Association
  • (PMID = 15451899.001).
  • [ISSN] 0149-5992
  • [Journal-full-title] Diabetes care
  • [ISO-abbreviation] Diabetes Care
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Insulin; 0 / Insulin Antibodies
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