β-cell failure in type 2 diabetes mellitus
Tóm tắt
Diabetes mellitus has been defined as a “group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both” and encompasses a wide range of heterogeneous conditions. Common type 2 diabetes mellitus (T2DM) results from a combination of genetic and acquired factors. However, lifestyle factors, particularly overeating and physical inactivity, are the major clinical determinants of T2DM. Insulin resistance is a common feature of T2DM, but it is unlikely to cause T2DM unless progressive loss of β-cell function develops. Significant reduction in β-cell function is already present at the time of T2DM diagnosis, and it continuously declines irrespective of treatment. As such, the progressive loss of β-cell function dictates the rate of worsened glycemic control. Development of progressive deterioration accelerates via gluco-and lipotoxicity, loss of β-cell function, and shrinkage of β-cell mass. Understanding the causes for β-cell failure is therefore of capital importance to develop new and more effective therapeutic strategies.
Tài liệu tham khảo
Del Prato S, Marchetti P, Bonadonna RC: Phasic insulin release and metabolic regulation in type 2 diabetes. Diabetes 2002, 51(Suppl 1):S109–S116.
Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998, 352:837–853.
U.K. prospective diabetes study 16. Overview of 6 years’ therapy of type II diabetes: a progressive disease. U.K. Prospective Diabetes Study Group. Diabetes 1995, 19:125–129.
Levy J, Atkinson AB, Bell PM, et al.: Beta-cell deterioration determines the onset and rate of progression of secondary dietary failure in type 2 diabetes mellitus: the 10-year follow-up of the Belfast Diet Study. Diabet Med 1998, 15:290–296.
Lencioni C, Volpe L, Miccoli R, et al.: Early impairment of beta-cell function and insulin sensitivity characterizes normotolerant Caucasian women with previous gestational diabetes. Nutr Metab Cardiovasc Dis 2006, 16:485–493.
Guiot Y, Sempoux C, Moulin P, Rahier J: No decrease of the beta-cell mass in type 2 diabetic patients. Diabetes 2001, 50(Suppl 1):S188.
Stefan Y, Orci L, Malaisse-Lagae F, et al.: Quantitation of endocrine cell content in the pancreas of nondiabetic and diabetic humans. Diabetes 1982, 31:694–700.
Del Guerra S, Lupi R, Marselli L, et al.: Functional and molecular defects of pancreatic islets in human type 2 diabetes. Diabetes 2005, 54:727–735.
Marchetti P, Del Guerra S, Marselli L, et al.: Pancreatic islets from type 2 diabetic patients have functional defects and increased apoptosis that are ameliorated by metformin. J Clin Endocrinol Metab 2004, 89:5535–5541.
Butler AE, Janson J, Bonner-Weir S, et al.: Beta-cell deficit and increased beta-cell apoptosis in humans with type 2 diabetes. Diabetes 2003, 52:102–110.
Florez JC: The new type 2 diabetes gene TCF7L2. Curr Opin Clin Nutr Metab Care 2007, 10:391–396.
Schäfer SA, Tschritter O, Machicao F, et al.: Impaired glucagon-like peptide-1-induced insulin secretion in carriers of transcription factor 7-like 2 (TCF7L2) gene polymorphisms. Diabetologia 2007, 50:2443–2450.
Lyssenko V, Lupi R, Marchetti P, et al.: Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes. J Clin Invest 2007, 117:2155–2163.
Kaiser N, Leibowitz G, Nesher R: Glucotoxicity and beta-cell failure in type 2 diabetes mellitus. J Pediatr Endocrinol Metab 2003, 16:5–22.
Del Guerra S, Grupillo M, Masini M, et al.: Gliclazide protects human islet beta-cells from apoptosis induced by intermittent high glucose. Diabetes Metab Res Rev 2007, 23:234–238.
D’Alessandris C, Andreozzi F, Federici M, et al.: Increase O-glycosylation of insulin signaling proteins results in their impaired activation and enhanced susceptibility to apoptosis in pancreatic beta-cells. FASEB J 2004, 18:959–961.
Kulkarni RN: Receptors for insulin and insulin-like growth factor-1 and insulin receptor substrate-1 mediate pathways that regulate islet function. Biochem Soc Trans 2002, 30:317–322.
Harding HP, Ron D: Endoplasmic reticulum stress and the development of diabetes: a review. Diabetes 2002, 51:S455–S461.
Zhang K, Kaufman RJ: Protein folding in the endoplasmic reticulum and the unfolded protein response. Handb Exp Pharmacol 2006, 172:69–91.
Marchetti P, Bugliani M, Lupi R, et al.: The endoplasmic reticulum in pancreatic beta cells of type 2 diabetes patients. Diabetologia 2007, 50:2486–2494.
Yudkin JS: Adipose tissue, insulin action and vascular disease: inflammatory signals. Int J Obes Relat Metab Disord 2003, 27(Suppl 3):S25–S28.
Maedler K, Sergeev P, Ehses JA, et al.: Leptin modulates beta cell expression of IL-1 receptor antagonist and release of IL-1beta in human islets. Proc Natl Acad Sci U S A 2004, 101:8138–8143.
Donath MY, Storling J, Maedler K, Mandrup-Poulsen T: Inflammatory mediators and islets beta-cell failure: a link between type 1 and type 2 diabetes. J Mol Med 2003, 81:455–470.
DeFronzo RA: Dysfunctional fat cells, lipotoxicity and type 2 diabetes. Int J Clin Pract 2004, 143:9–21.
Shimabukuro M, Wang MY, Zhou YT, et al.: Protection against lipoapoptosis of beta cells through leptin-dependent maintenance of Bcl-2 expression. Proc Natl Acad Sci U S A 1998, 95:9558–9561.
McGarry JD, Dobbins RL: Fatty acids, lipotoxicity and insulin secretion. Diabetologia 1999, 42:128–138.
Poitout V, Robertson RP: Glucolipotoxicity: fuel excess and beta-cell dysfunction. Endocr Rev 2007 Nov 29 (Epub ahead of print).
Gravena C, Mathias PC, Ashcroft SJ: Acute effects of fatty acids on insulin secretion from rat and human islets of Langerhans. J Endocrinol 2002, 173:73–80.
Lupi R, Dotta F, Marselli L, et al.: Prolonged exposure to free fatty acids has cytostatic and pro-apoptotic effects on human pancreatic islets: evidence that beta-cell death is caspase mediated, partially dependent on ceramide pathway, and Bcl-2 regulated. Diabetes 2002, 51:1437–1442.
Wrede CE, Dickson LM, Lingohr MK, et al.: Protein kinase B/Akt prevents fatty acid-induced apoptosis in pancreatic beta-cells (INS-1). J Biol Chem 2002, 277:49676–49684.
Shimabukuro M, Zhou YT, Levi M, Unger RH: Fatty acid-induced beta cell apoptosis: a link between obesity and diabetes. Proc Natl Acad Sci U S A 1998, 95:2498–2502.
Shimabukuro M, Ohneda M, Lee Y, Unger RH: Role of nitric oxide in obesity induced beta cell disease. J Clin Invest 1997, 100:290–295.
Maedler K, Oberholzer J, Bucher P, et al.: Monounsaturated fatty acids prevent the deleterious effects of palmitate and high glucose on human pancreatic beta-cell turnover and function. Diabetes 2003, 52:726–733.
Lukinius A, Wilander E, Westermark GT, et al.: Co-localization of islet amyloid polypeptide and insulin in the B cell secretory granules of the human pancreatic islets. Diabetologia 1989, 32:240–244.
Höppener JWM, Lips CJM: Role of islet amyloid in type 2 diabetes mellitus. Int J Biochem Cell Biol 2006, 38:726–736.
Finegood D, Topp B: Beta-cell deterioration—prospects for reversal or prevention. Diabetes Obes Metab 2001, 3:S20–S27.
Hayden M, Tyagi S: Islet redox stress: the manifold toxicities of insulin resistance, metabolic syndrome and amylin derived islet amyloid in type 2 diabetes mellitus. Pancreas 2002, 3:86–108.
Janson J, Ashley R, Harrison D, et al.: The mechanism of islet amyloid polypeptide toxicity is membrane disruption by intermediate-sized toxic amyloid particles. Diabetes 1999, 48:491–498.
Lorenzo A, Razzaboni B, Weir GC, Yankner BA: Pancreatic islet cell toxicity of amylin associated with type-2 diabetes mellitus. Nature 1994, 368:756–760.
Wang F, Hull R, Vidal J, et al.: Islet amyloid develops diffusely throughout the pancreas before becoming severe and replacing endocrine cells. Diabetes 2001, 50:2514–2520.
Takahashi A, Nagashima K, Hamasaki A, et al.: Sulfonylurea and glinide reduce insulin content, functional expression of K(ATP) channels, and accelerate apoptotic beta-cell death in the chronic phase. Diabetes Res Clin Pract 2007, 77:343–350.
Maedler K, Carr RD, Bosco D, et al.: Sulfonylurea induced beta-cell apoptosis in cultured human islets. J Clin Endocrinol Metab 2005, 90:501–506.
Del Guerra S, Marselli L, Lupi R, et al.: Effects of prolonged in vitro exposure to sulphonylureas on the function and survival of human islets. J Diabetes Complications 2005, 19:60–64.
Drucker DJ, Nauk MA: The incretin system: glucagon-like peptide 1 receptor agonists and dipeptidyl peptidase-4 inhibitors in type 2 diabetes. Lancet 2006, 368:1696–1705.
Perfetti R, Hui H: The role of GLP-1 in the life and death of pancreatic beta-cell. Horm Metab Res 2004, 36:804–810.
Del Prato S, Marchetti P: Targeting insulin resistance and beta-cell dysfunction: the role of thiazolidinediones. Diabetes Technol Ther 2004, 6:719–731.
Lupi R, Del Guerra S, Marselli L, et al.: Rosiglitazone prevents the impairment of human islet function induced by fatty acids: evidence for a role of PPARgamma2 in the modulation of insulin secretion. Am J Physiol Endocrinol Metab 2004, 286:E560–E567.
Del Prato S, Wishner WJ, Gromada J, Schluchter BJ: Beta-cell mass plasticity in type 2 diabetes. Diabetes Obes Metab 2004, 6:319–331.
Del Prato S, Bianchi C, Marchetti P: Beta-cell function and anti-diabetic pharmacotherapy. Diabetes Metab Res Rev 2007, 23:518–527.