Effects of the antitumor drug OSI-906, a dual inhibitor of IGF-1 receptor and insulin receptor, on the glycemic control, β-cell functions, and β-cell proliferation in male mice

Endocrinology

Volumn 155, Issue 6, 2014, Pages 2102-2111

  Shirakawa, Jun ^a   Okuyama, Tomoko ^a   Yoshida, Eiko ^a   Shimizu, Mari ^a   Horigome, Yuka ^a   Tuno, Takayuki ^a   Hayasaka, Moe ^a   Abe, Shiori ^a   Fuse, Masahiro ^a   Togashi, Yu ^a   Terauchi, Yasuo ^a  

^a YOKOHAMA CITY UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

GLUCOKINASE; GLUCOSE; INSULIN; INSULIN RECEPTOR; INSULIN RECEPTOR SUBSTRATE 2; LINSITINIB; PHLORIZIN; SOMATOMEDIN C RECEPTOR; 3-(8-AMINO-1-(2-PHENYLQUINOLIN-7-YL)IMIDAZO(1,5-A)PYRAZIN-3-YL)-1-METHYLCYCLOBUTANOL; GLUCOSE BLOOD LEVEL; IMIDAZOLE DERIVATIVE; PYRAZINE DERIVATIVE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CELL PROLIFERATION; CONTROLLED STUDY; DIABETIC PATIENT; DISEASE EXACERBATION; DOSE RESPONSE; DRUG EFFECT; DRUG EFFICACY; GLUCOSE INTOLERANCE; GLUCOSE TOLERANCE; GLYCEMIC CONTROL; HYPERGLYCEMIA; HYPERINSULINEMIA; IN VITRO STUDY; INSULIN RELEASE; INSULIN RESISTANCE; MALE; MOUSE; NONHUMAN; OBESITY; PANCREAS ISLET BETA CELL; PRIORITY JOURNAL; WILD TYPE; ANIMAL; ANTAGONISTS AND INHIBITORS; C57BL MOUSE; CYTOLOGY; DRUG EFFECTS; GLUCOSE BLOOD LEVEL; GLUCOSE TOLERANCE TEST; METABOLISM; REAL TIME POLYMERASE CHAIN REACTION;

ANIMALS; BLOOD GLUCOSE; CELL PROLIFERATION; GLUCOSE TOLERANCE TEST; IMIDAZOLES; INSULIN-SECRETING CELLS; MALE; MICE; MICE, INBRED C57BL; PYRAZINES; REAL-TIME POLYMERASE CHAIN REACTION; RECEPTOR, IGF TYPE 1; RECEPTOR, INSULIN;

EID: 84901449316     PISSN: 00137227     EISSN: 19457170     Source Type: Journal    
DOI: 10.1210/en.2013-2032     Document Type: Article

References (36)

1. Giovannucci E, Harlan DM, Archer MC, et al. Diabetes and cancer: a consensus report. Diabetes Care. 2010;33: 1674-1685.
2. Bowker SL, Majumdar SR, Veugelers P, Johnson JA. Increased cancer-related mortality for patients with type 2 diabetes who use sulfonylureas or insulin: Response to Farooki and Schneider. Diabetes Care. 2006;29: 1990-1991.
3. Kulkarni RN, Brüning JC, Winnay JN, Postic C, Magnuson MA, Kahn CR. Tissue-specific knockout of the insulin receptor in pancreatic β-cells creates an insulin secretory defect similar to that in type 2 diabetes. Cell. 1999;96: 329-339.
4. Kulkarni RN, Holzenberger M, Shih DQ, et al. β-Cell-specific deletion of the Igf1 receptor leads to hyperinsulinemia and glucose intolerance but does not alterβ-cell mass. Nat Genet. 2002;31: 111-115.
5. Ueki K, Okada T, Hu J, et al. Total insulin and IGF-I resistance in pancreatic β-cells causes overt diabetes. Nat Genet. 2006;38: 583-588.
6. Weinstein D, Simon M, Yehezkel E, Laron Z, Werner H. Insulin analogues display IGF-I-like mitogenic and anti-apoptotic activities in cultured cancer cells. Diabetes Metab Res Rev. 2009;25: 41-49.
7. Mulvihill MJ, Cooke A, Rosenfeld-Franklin M, et al. Discovery of OSI-906: a selective and orally efficacious dual inhibitor of the IGF-1 receptor and insulin receptor. Future Med Chem. 2009;1: 1153-1171.
8. Kuhn DJ, Berkova Z, Jones RJ, et al. Targeting the insulin-like growth factor-1 receptor to overcome bortezomib resistance in preclinical models of multiple myeloma. Blood. 2012;120: 3260-3270.
9. Fox EM, Miller TW, Balko JM, et al. A kinome-wide screen identifies the insulin/IGF-I receptor pathway as a mechanism of escape from hormone dependence in breast cancer. Cancer Res. 2011;71: 6773-6784.
10. McKinley ET, Bugaj JE, Zhao P, et al. 18FDG-PET predicts pharmacodynamic response to OSI-906, a dual IGF-1R/IR inhibitor, in preclinical mouse models of lung cancer. Clin Cancer Res. 2011; 17: 3332-3340.
11. Kim WY, Prudkin L, Feng L, et al. Epidermal growth factor receptor and K-Ras mutations and resistance of lung cancer to insulin-like growth factor 1 receptor tyrosine kinase inhibitors. Cancer. 2012; 118: 3993-4003.
12. Terauchi Y, Sakura H, Yasuda K, et al. Pancreatic β-cell-specific targeted disruption of glucokinase gene. Diabetes mellitus due to defective insulin secretion to glucose. J Biol Chem. 1995;270: 30253-30256.
13. Kubota N, Tobe K, Terauchi Y, et al. Disruption of insulin receptor substrate 2 causes type 2 diabetes because of liver insulin resistance and lack of compensatory β-cell hyperplasia. Diabetes. 2000;49: 1880-1889.
14. Okada T, Liew CW, Hu J, et al. Insulin receptors in β-cells are critical for islet compensatory growth response to insulin resistance. Proc Natl Acad Sci U S A. 2007;104: 8977-8982.
15. Yi P, Park JS, Melton DA. Betatrophin: a hormone that controls pancreatic β-cell proliferation. Cell. 2013;153: 747-758.
16. Terauchi Y, TakamotoI, Kubota N, et al. Glucokinase and IRS-2 are required for compensatoryβ-cell hyperplasia in response to high-fat diet-induced insulin resistance. J Clin Invest. 2007;117: 246-257.
17. Shirakawa J, Amo K, Ohminami H, et al. Protective effects of dipeptidyl peptidase-4 (DPP-4) inhibitor against increased β-cell ap-optosis induced by dietary sucrose and linoleic acid in mice with diabetes. J Biol Chem. 2011;286: 25467-25476.
18. King ER, WongKK.Insulin-like growth factor: current concepts and new developments in cancer therapy. Recent Pat Anticancer Drug Discov. 2012;7: 14-30.
19. Shirakawa J, Tanami R, Togashi Y, et al. Effects of liraglutide on β-cell-specific glucokinase-deficient neonatal mice. Endocrinology. 2012;153: 3066-3075.
20. Shirakawa J, Togashi Y, Sakamoto E, et al. Glucokinase activation ameliorates ER stress-induced apoptosis in pancreatic β-cells. Diabetes. 2013;62: 3448-3458.
21. Salpeter SJ, Klein AM, Huangfu D, Grimsby J, Dor Y. Glucose and aging control the quiescence period that follows pancreatic β-cell replication. Development. 2010;137: 3205-3213.
22. Nakamura A, Togashi Y, Orime K, et al. Control of β-cell function and proliferation in mice stimulated by small-molecule glucokinase activator under various conditions. Diabetologia. 2012;55: 1745-1754.
23. Anisimov VN, Berstein LM, Popovich IG, et al. Central and peripheral effects of insulin/IGF-1 signaling in aging and cancer: antidiabetic drugs as geroprotectors and anticarcinogens. Ann N Y Acad Sci. 2005;1057: 220-234.
24. Belfiore A, Frasca F, Pandini G, Sciacca L, Vigneri R. Insulin receptor isoforms and insulin receptor/insulin-like growth factor receptor hybrids in physiology and disease. Endocr Rev. 2009;30: 586-623.
25. Zeng X, Zhang H, Oh A, Zhang Y, Yee D. Enhancement of doxorubicin cytotoxicity of human cancer cells by tyrosine kinase inhibition of insulin receptor and type I IGF receptor. Breast Cancer Res Treat. 2012;133: 117-126.
26. Goldfine AB, Kulkarni RN. Modulation of β-cell function: a translational journey from the bench to the bedside. Diabetes Obes Metab. 2012;14(Suppl 3): 152-160.
27. Leibiger IB, Leibiger B, Berggren PO. Insulin signaling in the pancreatic β-cell. Annu Rev Nutr. 2008;28: 233-251.
28. White MF. Regulating insulin signaling and β-cell function through IRS proteins. Can J Physiol Pharmacol. 2006;84: 725-737.
29. Rhodes CJ. Type 2 diabetes-A matter ofβ-cell life and death? Science. 2005;307: 380-384.
30. El Ouaamari A, Kawamori D, Dirice E, et al. Liver-derived systemic factors drive β-cell hyperplasia in insulin-resistant states. Cell Rep. 2013;3: 401-410.
31. Dirice E, Kahraman S, Jiang W, et al. Soluble factors secreted by T cells promote β-cell proliferation. Diabetes. 2014;63: 188-202.
32. Salpeter SJ, Khalaileh A, Weinberg-Corem N, Ziv O, Glaser B, Dor Y. Systemic regulation of the age-related decline of pancreatic β-cell replication. Diabetes. 2013;62: 2843-2848.
33. Togashi Y, Shirakawa J, Orime K, et al. β-Cell proliferation after a partial pancreatectomy is independent of IRS-2 in mice. Endocrinology. 2014;155: 1643-1652.
34. Rhodes CJ, White MF, Leahy JL, Kahn SE. Direct autocrine action of insulin on β-cells: does it make physiological sense? Diabetes. 2013;62: 2157-2163.
35. Talchai C, Xuan S, Lin HV, Sussel L, Accili D. Pancreatic β-cell dedifferentiation as a mechanism of diabetic β-cell failure. Cell. 2012;150: 1223-1234.
36. Thorel F, Népote V, Avril I, et al. Conversion of adult pancreatic alpha-cells to β-cells after extreme β-cell loss. Nature. 2010;464: 1149-1154.