¿Por qué fallan las células ß? | 15 JUN 15

Secreción de insulina y diabetes tipo 2

La alteración de la secreción de insulina podría deberse a una disminución de la tasa de secreción celular o a una disminución de la masa de las células β o a ambos. Se analizan en profundidad los mecanismos íntimos del proceso.
Autor/a: James Cantley, Frances M. Ashcroft Fuente: BMC Biology (2015) 13:33 Insulin secretion and type 2 diabetes: why do β-cells fail?
INDICE:  1.  | 2. Referencias
Referencias

1. UK Prospective Diabetes Study (UKPDS) Group. Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Lancet. 1998;352:837–53.
2. Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54:1615–25.
3. Forbes JM, Cooper ME. Mechanisms of diabetic complications. Physiological Reviews, Volume 93. 2013;1:137–88.
4. International Diabetes Federation. IDF Diabetes Atlas. 6th edition. 2013.
5. Ray JA, Valentine WJ, Secnik K, Oglesby AK, Cordony A, Gordois A, et al. Review of the cost of diabetes complications in Australia, Canada, France, Germany, Italy and Spain. Curr Med Res Opin. 2005;21:1617–29.
6. Scully T. Diabetes in numbers. Nature. 2012;485:S2–3. 7. Kahn SE. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes. Diabetologia. 2003;46:3–19.
8. Oram R, Jones A, Besser RJ, Knight B, Shields B, Brown R, et al. The majority of patients with long-duration type 1 diabetes are insulin microsecretors and have functioning beta cells. Diabetologia. 2014;57:187–91.
9. Quintens R, Hendrickx N, Lemaire K, Schuit F. Why expression of some genes is disallowed in beta-cells. Biochem Soc Trans. 2008;36:300–5.
10. Pullen TJ, Khan AM, Barton G, Butcher SA, Sun G, Rutter GA. Identification of genes selectively disallowed in the pancreatic islet. Islets. 2010;2:89–95.
11. Schuit F, Van Lommel L, Granvik M, Goyvaerts L, de Faudeur G, Schraenen A, et al. β-cell-specific gene repression: a mechanism to protect against inappropriate or maladjusted insulin secretion? Diabetes. 2012;61:969–75.
12. Otonkoski T, Jiao H, Kaminen-Ahola N, Tapia-Paez I, Ullah MS, Parton LE, et al. Physical exercise-induced hypoglycemia caused by failed silencing of monocarboxylate transporter 1 in pancreatic beta cells. Am J Hum Genet. 2007;81:467–74.
13. Pullen TJ, Sylow L, Sun G, Halestrap AP, Richter EA, Rutter GA. Overexpression of monocarboxylate transporter-1 (Slc16a1) in mouse pancreatic β-cells leads to relative hyperinsulinism during exercise. Diabetes. 2012;61:1719–25.
14. Kulkarni RN, Stewart AF. Summary of the Keystone Islet Workshop (April. 2014): the increasing demand for human islet availability in diabetes research. Diabetes. 2014;63:3979–81.
15. Cantley J, Walters SN, Jung MH, Weinberg A, Cowley MJ, Whitworth TP, et al. A preexistent hypoxic gene signature predicts impaired islet graft function and glucose homeostasis. Cell Transplant. 2013;22:2147–59.
16. Deng S, Vatamaniuk M, Huang X, Doliba N, Lian M-M, Frank A, et al. Structural and functional abnormalities in the islets isolated from type 2 diabetic subjects. Diabetes. 2004;53:624–32.
17. Marselli L, Suleiman M, Masini M, Campani D, Bugliani M, Syed F, et al. Are we overestimating the loss of beta cells in type 2 diabetes? Diabetologia. 2014;57:362–5.
18. Rosengren AH, Braun M, Mahdi T, Andersson SA, Travers ME, Shigeto M, et al. Reduced insulin exocytosis in human pancreatic beta-cells with gene variants linked to type 2 diabetes. Diabetes. 2012;61:1726–33.
19. Butler AE, Janson J, Bonner-Weir S, Ritzel R, Rizza RA, Butler PC. Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003;52:102–10.
20. Yoon KH, Ko SH, Cho JH, Lee JM, Ahn YB, Song KH, et al. Selective beta-cell loss and alpha-cell expansion in patients with type 2 diabetes mellitus in Korea. J Clin Endocrinol Metab. 2003;88:2300–8.
21. Rahier J, Guiot Y, Goebbels RM, Sempoux C, Henquin JC. Pancreatic β-cell mass in European subjects with type 2 diabetes. Diabetes Obesity Metab. 2008;10:32–42.
22. Brereton MF, Iberl M, Shimomura K, Zhang Q, Adriaenssens AE, Proks P, et al. Reversible changes in pancreatic islet structure and function produced by elevated blood glucose. Nat Commun. 2014;5:4639.
23. Weir GC, Aguayo-Mazzucato C, Bonner-Weir S. Beta-cell dedifferentiation in diabetes is important, but what is it? Islets. 2013;5:233–7.
24. Talchai C, Xuan S, Lin Hua V, Sussel L, Accili D. Pancreatic β cell dedifferentiation as a mechanism of diabetic β cell failure. Cell. 2012;150:1223–34.
25. Wang Z, York NW, Nichols CG, Remedi MS. Pancreatic beta cell dedifferentiation in diabetes and redifferentiation following insulin therapy. Cell Metab. 2014;19:872–82.
26. Guo S, Dai C, Guo M, Taylor B, Harmon JS, Sander M, et al. Inactivation of specific beta cell transcription factors in type 2 diabetes. J Clin Investig. 2013;123:3305–16.
27. Fiori JL, Shin Y-K, Kim W, Krzysik-Walker SM, González-Mariscal I, Carlson OD, et al. Resveratrol prevents β-cell dedifferentiation in nonhuman primates given a high-fat/high-sugar diet. Diabetes. 2013;62:3500–13.
28. Thorel F, Nepote V, Avril I, Kohno K, Desgraz R, Chera S, et al. Conversion of adult pancreatic alpha-cells to beta-cells after extreme beta-cell loss. Nature. 2010;464:1149–54.
29. Chera S, Baronnier D, Ghila L, Cigliola V, Jensen JN, Gu G, et al. Diabetes recovery by age-dependent conversion of pancreatic δ-cells into insulin producers. Nature. 2014;514:503–7.
30. Yach D, Stuckler D, Brownell KD. Epidemiologic and economic consequences of the global epidemics of obesity and diabetes. Nat Med. 2006;12:62–6.
31. Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature. 2006;444:840–6.
32. Hu FB. Globalization of diabetes: the role of diet, lifestyle, and genes. Diabetes Care. 2011;34:1249–57.
Cantley and Ashcroft BMC Biology (2015) 13:33 Page 6 of 7 33. Perley M, Kipnis DM. Plasma insulin responses to glucose and tolbutamide of normal weight and obese diabetic and nondiabetic subjects. Diabetes. 1966;15:867–74.
34. Polonsky KS, Given BD, Van Cauter E. Twenty-four-hour profiles and pulsatile patterns of insulin secretion in normal and obese subjects. J Clin Investig. 1988;81:442–8.
35. Saisho Y, Butler AE, Manesso E, Elashoff D, Rizza RA, Butler PC. β-cell mass and turnover in humans: effects of obesity and aging. Diabetes Care. 2013;36:111–7.
36. Medici F, Hawa M, Ianari A, Pyke DA, Leslie RDG. Concordance rate for Type II diabetes mellitus in monozygotic twins: actuarial analysis. Diabetologia. 1999;42:146–50.
37. Lyssenko V, Almgren P, Anevski D, Perfekt R, Lahti K, Nissén M, et al. Predictors of and longitudinal changes in insulin sensitivity and secretion preceding onset of type 2 diabetes. Diabetes. 2005;54:166–74.
38. Volkmar M, Dedeurwaerder S, Cunha DA, Ndlovu MN, Defrance M, Deplus R, et al. DNA methylation profiling identifies epigenetic dysregulation in pancreatic islets from type 2 diabetic patients. EMBO J. 2012;31:1405–26.
39. Sandovici I, Smith NH, Nitert MD, Ackers-Johnson M, Uribe-Lewis S, Ito Y, et al. Maternal diet and aging alter the epigenetic control of a promoter-enhancer interaction at the Hnf4a gene in rat pancreatic islets. Proc Natl Acad Sci U S A. 2011;108:5449–54.
40. Ng SF, Lin RC, Laybutt DR, Barres R, Owens JA, Morris MJ. Chronic high-fat diet in fathers programs beta-cell dysfunction in female rat offspring. Nature. 2010;467:963–6.
41. Fernandez-Twinn DS, Ozanne SE. Mechanisms by which poor early growth programs type-2 diabetes, obesity and the metabolic syndrome. Physiol Behav. 2006;88:234–43.
42. Dabelea D, Crume T. Maternal environment and the transgenerational cycle of obesity and diabetes. Diabetes. 2011;60:1849–55.
43. Lyssenko V, Laakso M. Genetic screening for the risk  f type 2 diabetes: worthless or valuable? Diabetes Care. 2013;36:S120–6.
44. Gloyn AL, Pearson ER, Antcliff JF, Proks P, Bruining GJ, Slingerland AS, et al. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med. 2004;350:1838–49.
45. Mahajan A, Go MJ, Zhang W, Below JE, Gaulton KJ, Ferreira T, et al. Genome-wide trans-ancestry meta-analysis provides insight into the genetic architecture of type 2 diabetes susceptibility. Nat Genet. 2014;46:234–44.
46. Dimas AS, Lagou V, Barker A, Knowles JW, Mägi R, Hivert M-F, et al. Impact of type 2 diabetes susceptibility variants on quantitative glycemic traits reveals mechanistic heterogeneity. Diabetes. 2014;63:2158–71.
47. Couch FJ, Nathanson KL, Offit K. Two decades after BRCA: setting paradigms in personalized cancer care and prevention. Science. 2014;343:1466–70.
48. Pearson ER, Flechtner I, Njolstad PR, Malecki MT, Flanagan SE, Larkin B, et al. Switching from insulin to oral sulfonylureas in patients with diabetes due to Kir6.2 mutations. N Engl J Med. 2006;355:467–77.
49. Tang Y, Axelsson AS, Spegel P, Andersson LE, Mulder H, Groop LC, et al. Genotype-based treatment of type 2 diabetes with an alpha2A-adrenergic receptor antagonist. Sci Transl Med. 2014;6:257ra139.
50. Ashcroft FM, Rorsman P. K(ATP) channels and islet hormone secretion: new insights and controversies. Nat Rev Endocrinol. 2013;9:660–9.
51. Lee Y, Berglund ED, Wang MY, Fu X, Yu X, Charron MJ, et al. Metabolic manifestations of insulin deficiency do not occur without glucagon action. Proc Natl Acad Sci U S A. 2012;109:14972–6.
52. Miller RA, Chu Q, Xie J, Foretz M, Viollet B, Birnbaum MJ. Biguanides suppress hepatic glucagon signalling by decreasing production of cyclic AMP. Nature. 2013;494:256–60.
53. Prince MJ, Garhyan P, Abu-Raddad EJ, Fu H, Lim CN, Pinaire JA, et al. Short-term treatment with glucagon receptor antagonist LY2409021 effectively reduces fasting blood glucose (FBG) and HbA1c in patients with type 2 diabetes mellitus. Diabetologia. 2011;54:S86.
54. Nauck MA, Vilsbøll T, Gallwitz B, Garber A, Madsbad S. Incretin-based therapies: viewpoints on the way to consensus. Diabetes Care. 2009;32:S223–31.
55. Lim EL, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia. 2011;54:2506–14.
56. Weng J, Li Y, Xu W, Shi L, Zhang Q, Zhu D, et al. Effect of intensive insulin therapy on beta-cell function and glycaemic control in patients with newly diagnosed type 2  diabetes: a multicentre randomised parallel-group trial. Lancet. 2008;371:1753–60.
57. Kramer CK, Choi H, Zinman B, Retnakaran R. Determinants of reversibility of beta-cell dysfunction in response to short-term intensive insulin therapy in patients with early type 2 diabetes. Am J Physiol Endocrinol Metab. 2013;305:E1398–407.
58. Parkes DG, Pittner R, Jodka C, Smith P, Young A. Insulinotropic actions of exendin-4 and glucagon-like peptide-1 in vivo and in vitro. Metabolism. 2001;50:583–9. 59. Nauck MA. A critical analysis of the clinical use of incretin-based therapies: the benefits by far outweigh the potential risks. Diabetes Care. 2013;36:2126–32.
60. Gale EA. GLP-1 based agents and acute pancreatitis: drug safety falls victim to the three monkey paradigm. BMJ. 2013;346:f1263.
61. Butler PC, Elashoff M, Elashoff R, Gale EAM. A critical analysis of the clinical use of incretin-based therapies: are the GLP-1 therapies safe? Diabetes Care. 2013;36:2118–25.
62. Chandarana K, Batterham RL. Shedding pounds after going under the knife: metabolic insights from cutting the gut. Nat Med. 2012;18:668–9.
63. Chambers AP, Jessen L, Ryan KK, Sisley S, Wilson-Perez HE, Stefater MA, et al. Weight-independent changes in blood glucose homeostasis after gastric bypass or vertical sleeve gastrectomy in rats. Gastroenterology. 2011;141:950–8.

 

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