Increasing β-cell mass requires additional stimulation for adaptation to secretory demand

Molecular Endocrinology

Volumn 29, Issue 1, 2015, Pages 108-120

  Mondal, Prosenjit ^a,b   Song, Woo Jin ^a   Li, Yuanyuan ^a,c   Yang, Kil S ^a   Hussain, Mehboob A ^a  

^a JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b SCRIPPS RESEARCH INSTITUTE   (United States)

^c NORTHEAST OHIO MEDICAL UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CYCLIN A2; EXENDIN 4; GLUCOSE TRANSPORTER 1; INSULIN; PROTEIN P27; RETINOBLASTOMA PROTEIN; S PHASE KINASE ASSOCIATED PROTEIN 2; TRANSCRIPTION FACTOR MAFA; TRANSCRIPTION FACTOR NKX6.1; TRANSCRIPTION FACTOR PDX 1; CCNA2 PROTEIN, MOUSE; GLP1R PROTEIN, MOUSE; GLUCAGON LIKE PEPTIDE 1 RECEPTOR; GLUCOSE;

ADULT; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL DIFFERENTIATION; CELL MEMBRANE DEPOLARIZATION; CELL PROLIFERATION; CELL STIMULATION; CELLULAR PARAMETERS; CONTROLLED STUDY; DIABETOGENESIS; EXOCYTOSIS; GLUCOSE HOMEOSTASIS; GLUCOSE INTOLERANCE; GLUCOSE TOLERANCE; GLYCEMIC CONTROL; IMMUNOREACTIVITY; IN VIVO STUDY; INSULIN RELEASE; LIPID DIET; MOUSE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; PANCREAS ISLET BETA CELL; PANCREAS ISLET BETA CELL MASS; PANCREAS ISLET CELL FUNCTION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; STIMULUS SECRETION COUPLING; UPREGULATION; ANIMAL; BIOSYNTHESIS; C57BL MOUSE; CELL COUNT; CYTOLOGY; DEFICIENCY; GENETICS; GLUCOSE TOLERANCE TEST; METABOLISM; PANCREAS; TRANSGENIC MOUSE;

MUS;

ANIMALS; CELL COUNT; CELL PROLIFERATION; CYCLIN A2; DIABETES MELLITUS, TYPE 2; DIET, HIGH-FAT; GLUCAGON-LIKE PEPTIDE-1 RECEPTOR; GLUCOSE; GLUCOSE INTOLERANCE; GLUCOSE TOLERANCE TEST; INSULIN; INSULIN-SECRETING CELLS; MICE; MICE, INBRED C57BL; MICE, TRANSGENIC; PANCREAS;

EID: 84922270412     PISSN: 08888809     EISSN: 19449917     Source Type: Journal    
DOI: 10.1210/me.2014-1265     Document Type: Article

References (41)

1. Henquin JC, et al. Pancreatic β-cell mass or β-cell function? That is the question! Diabetes Obes Metab. 2008;10(suppl 4):1- 4.
2. Stamateris RE, et al. Adaptive β-cell proliferation increases early in high-fat feeding in mice, concurrent with metabolic changes, with induction of islet cyclin D2 expression. Am J Physiol Endocrinol Metab. 2013;305(1):E149-E159.
3. Peyot M.L, et al. β-Cell failure in diet-induced obese mice stratified according to body weight gain: secretory dysfunction and altered islet lipid metabolism without steatosis or reduced β-cell mass. Diabetes. 2010;59(9):2178-2187.
4. Guo S, et al. Inactivation of specific β cell transcription factors in type 2 diabetes. J Clin Invest. 2013;123(8):3305-3316.
5. Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature. 2006;444(7121): 840-846.
6. Rahier J, et al. Pancreatic β-cell mass in European subjects with type 2 diabetes. Diabetes Obes Metab. 2008:10(suppl 4):32- 42.
7. Butler AE, et al. Increased β-cell apoptosis prevents adaptive increase in β-cell mass in mouse model of type 2 diabetes: evidence for role of islet amyloid formation rather than direct action of amyloid. Diabetes. 2003;52(9):2304-8414.
8. Butler AE, et al. β-Cell deficit and increased β-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003;52(1):102-110.
9. Gregg BE, et al. Formation of a human β-cell population within pancreatic islets is set early in life. J Clin Endocrinol Metab. 2012; 97(9):3197-206.
10. Meier JJ, et al. β-Cell replication is the primary mechanism subserving the postnatal expansion of β-cell mass in humans. Diabetes. 2008;57(6):1584-1594.
11. Prentki M, Nolan CJ. Islet β cell failure in type 2 diabetes. J Clin Invest. 2006;116(7):1802-1812.
12. de Koning EJ, Bonner-Weir S, Rabelink TJ. Preservation of β-cell function by targeting β-cell mass. Trends Pharmacol Sci. 2008; 29(4):218-227.
13. Bernal-Mizrachi E, et al. Human β-cell proliferation and intracellular signaling part 2: still driving in the dark without a road map. Diabetes. 2014;63(3):819-231.
14. Kulkarni RN, et al. Human β-cell proliferation and intracellular signaling: driving in the dark without a road map. Diabetes. 2012; 61(9):2205-2213.
15. Bernal-Mizrachi E, et al. Transgenic overexpression of active calcineurin in β-cells results in decreased β-cell mass and hyperglycemia. PLoS One. 2010;5(8):e11969.
16. Elghazi L, et al. Decreased IRS signaling impairs β-cell cycle progression and survival in transgenic mice overexpressing S6K in β-cells. Diabetes. 2010;59(10):2390-2399.
17. Favre D, et al. Role for inducible cAMP early repressor in promoting pancreatic β cell dysfunction evoked by oxidative stress in human and rat islets. Diabetologia. 2011;54(9):2337-23946.
18. Sander M, et al. Homeobox gene Nkx6.1 lies downstream of Nkx2.2 in the major pathway of β-cell formation in the pancreas. Development. 2000;127(24):5533-5540.
19. Zhang H, et al. Gestational diabetes mellitus resulting from impaired β-cell compensation in the absence of FoxM1, a novel downstream effector of placental lactogen. Diabetes. 2010;59(1):143- 152.
20. Zhong L, et al. Essential role of Skp2-mediated p27 degradation in growth and adaptive expansion of pancreatic β cells. J Clin Invest. 2007;117(10):2869-2876.
21. Rachdi L, et al. Disruption of Tsc2 in pancreatic β cells induces β cell mass expansion and improved glucose tolerance in a TORC1- dependent manner. Proc Natl Acad Sci USA. 2008;105(27):9250- 9255.
22. Butler M, et al. Specific inhibition of PTEN expression reverses hyperglycemia in diabetic mice. Diabetes. 2002;51(4):1028-1034.
23. Yang Y, et al. Reversal of preexisting hyperglycemia in diabetic mice by acute deletion of the Men1 gene. Proc Natl Acad Sci USA. 2010;107(47):20358-20363.
24. Stiles BL, et al. Selective deletion of Pten in pancreatic β cells leads to increased islet mass and resistance to STZ-induced diabetes. Mol Cell Biol. 2006;26(7):2772-2781.
25. Henley KD, et al. Inactivation of the dual Bmp/Wnt inhibitor Sostdc1 enhances pancreatic islet function. Am J Physiol Endocrinol Metab. 2012;303(6):E752-E761.
26. Kaihara KA, et al. β-Cell-specific protein kinase A activation enhances the efficiency of glucose control by increasing acute-phase insulin secretion. Diabetes. 2013;62(5):1527-1536.
27. Song WJ, et al. Pancreatic β-cell response to increased metabolic demand and to pharmacologic secretagogues requires EPAC2A. Diabetes. 2013;62(8):2796-2807.
28. Song WJ, et al. Snapin mediates incretin action and augments glucose- dependent insulin secretion. Cell Metab. 2011;13(3):308- 319.
29. Song WJ, et al. Exendin-4 stimulation of cyclin A2 in β-cell proliferation. Diabetes. 2008;57(9):2371-2381.
30. Drucker DJ. The biology of incretin hormones. Cell Metab. 2006; 3(3):153-165.
31. Berkovich I, Efrat S. Inducible and reversible β-cell autoimmunity and hyperplasia in transgenic mice expressing a conditional oncogene. Diabetes. 2001;50(10):2260-2267.
32. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-ΔΔC(T)) method. Methods. 2001;25(4):402-408.
33. Carrano AC, et al. SKP2 is required for ubiquitin-mediated degradation of the CDK inhibitor p27. Nat Cell Biol. 1999;1(4):193- 199.
34. Tschen SI, et al. Skp2 is required for incretin hormone-mediated β-cell proliferation. Mol Endocrinol. 2011;25(12):2134-2143.
35. Uchida T, et al. Deletion of Cdkn1b ameliorates hyperglycemia by maintaining compensatory hyperinsulinemia in diabetic mice. Nat Med. 2005;11(2):175-182.
36. Yusta B, et al. GLP-1 receptor activation improves β cell function and survival following induction of endoplasmic reticulum stress. Cell Metab. 2006;4(5):391-406.
37. Kieffer TJ, et al. Leptin suppression of insulin secretion by the activation of ATP-sensitive K+ channels in pancreatic β-cells. Diabetes. 1997;46(6):1087-1093.
38. Song WJ, et al. Glucagon regulates hepatic kisspeptin to impair insulin secretion. Cell Metab. 2014;19(4):667-681.
39. Smith EP, et al. The role of β cell glucagon-like peptide-1 signaling in glucose regulation and response to diabetes drugs. Cell Metab. 2014;19(6):1050-1057.
40. Nir T, Melton DA, Dor Y. Recovery from diabetes in mice by β cell regeneration. J Clin Invest. 2007;117(9):2553-2561.
41. Dor Y, et al. Adult pancreatic β-cells are formed by self-duplication rather than stem-cell differentiation. Nature. 2004;429(6987): 41-46.