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Original Articles

Palmitic acid-rich diet suppresses glucose-stimulated insulin secretion (GSIS) and induces endoplasmic reticulum (ER) stress in pancreatic islets in mice

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Pages 8-15 | Received 01 Jul 2014, Accepted 02 Apr 2015, Published online: 13 Jul 2015

References

  • International Diabetes Federation Diabetes Atlas. 3rd ed. Brussels, Belgium: International Diabetes Federation; 2006
  • Hossain P, Kawar B, El Nahas M. Obesity and diabetes in the developing world – a growing challenge. N Engl J Med 2007;356:213–15
  • Haffner SM, Lehto S, Rёnnemaa T, et al. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. N Engl J Med 1998;339:229–34
  • van Dam RM, Rimm EB, Willett WC, et al. Dietary patterns and risk for type 2 diabetes mellitus. Ann Intern Med 2002;136:201–9
  • Kahn SE. The relative contributions of insulin resistance and β-cell dysfunction to the pathophysiology of type 2 diabetes. Diabetologia 2003;46:3–19
  • Butler AE, Janson J, Bonner-Weir S, et al. β-Cell deficit and increased β-cell apoptosis in humans with type 2 diabetes. Diabetes 2003;52:102–10
  • McGarry JD, Dobbins RL. Fatty acids, lipotoxicity and insulin secretion. Diabetologia 1999;42:128–38
  • Kawai T, Hirose H, Seto Y, et al. Chronic effects of different fatty acids and leptin in INS-1 cell. Diabetes Res Clin Pract 2001;51:1–8
  • Boden G. Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Diabetes 1997;46:3–10
  • Maedler K, Spinas GA, Dyntar D, et al. Distinct effects of saturated and monosaturated fatty acids on β-cell turnover and function. Diabetes 2001;50:69–76
  • Harding HP, Novoa I, Zhang Y, et al. Regulated translation initiation controls stress-induced gene expression in mammalian cells. Mol Cell 2000;6:1099–108
  • Lipson KL, Fonseca SG, Ishigaki S, et al. Regulation of insulin biosynthesis in pancreatic beta cells by an endoplasmic reticulum-resident protein kinase IRE1. Cell Metab 2006;4:245–54
  • Kharroubi I, Ladriere L, Cardozo AK, et al. Free fatty acids and cytokines induce pancreatic β-cell apoptosis by different mechanisms: role of nuclear factor-кB and endoplasmic reticulum stress. Endocrinology 2004;145:5087–96
  • Karaskov E, Scott C, Zhang L, et al. Chronic palmitate but not oleate exposure induces endoplasmic reticulum stress, which may contribute to INS-1 pancreatic β-cell apoptosis. Endocrinology 2006;47:3398–407
  • Seto Y, Fujita H, Dan K, et al. Stimulating activity of A-4166 on insulin release in in situ hamster pancreatic perfusion. Pharmacology 1995;51:245–53
  • Robertson RP, Harmon J, Tran PO, Poitout V. Beta-cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes. Diabetes 2004;53:119–24
  • Unger RH. Lipotoxicity in the pathogenesis of obesity-dependent NIDDM. Genetic and clinical implications. Diabetes 1995;44:863–70
  • Unger RH, Zhou Y-T. Lipotoxicity of β-cells in obesity and in other causes of fatty acid spillover. Diabetes 2001;50:118–21
  • Haber EP, Procopio J, Carvalho CR, et al. New insights into fatty acid modulation of pancreatic beta-cell function. Int Rev Cytol 2006;248:1–41
  • Zhou YP, Grill VE. Palmitate-induced β-cell insensitivity to glucose is coupled to decreased pyruvate dehydrogenase activity and enhanced kinase activity in rat pancreatic islets. Diabetes 1995;44:394–9
  • 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;52:726–33
  • Watson ML, Macrae K, Marley AE, Hundal HS. Chronic effects of palmitate overload on nutrition-induced insulin secretion and autocrine signaling in pancreatic MIN6 beta cells. PLoS One 2011;6:e25975
  • Matsuzaka T, Shimano H, Yahagi N, et al. Crucial role of a long-chain fatty acid elongase, Elovl6, in obesity-induced insulin resistance. Nat Med 2007;13:1193–202
  • Assimacopoulos-Jeannet F, Thumelin S, Roche E, et al. Fatty acids rapidly induce the carnitine palmitoyltransferase 1 gene in the pancreatic β-cell line INS-1. J Biol Chem 1997;272:1659–64
  • Lipson KL, Fonseca SG, Urano F. Endoplasmic reticulum stress-induced apoptosis and autoimmunity in diabetes. Curr Mol Med 2006;6:71–7
  • Montane J, Cadavez L, Novials A. Stress and the inflammatory process: a major cause of pancreatic cell death in type 2 diabetes. Diabetes Metab Syndr Obes 2014;7:25–34
  • Esposito K, Maiorino MI, Ceriello A, Giugliano D. Prevention and control of type 2 diabetes by Mediterranean diet: a systematic review. Diabetes Res Clin Pract 2010;89:97–102
  • InterAct Consortium. Mediterranean diet and type 2 diabetes risk in the European prospective investigation into cancer and nutrition (EPIC) study: the InterAct project. Diabetes Care 2011;34:1913–18
  • Peng G, Li L, Liu Y, et al. Oleate blocks palmitate-induced abnormal lipid distribution, endoplasmic reticulum expansion and stress, and insulin resistance in skeletal muscle. Endocrinology 2011;152:2206–18
  • Wu HT, Chen W, Cheng KC, et al. Oleic acid activates peroxisome proliferator-activated receptor δ to compensate insulin resistance in steatotic cells. J Nutr Biochem 2012;23:1264–70
  • Tardif N, Salles J, Landrier J-F, et al. Oleate-enriched diet improves insulin sensitivity and restores muscle protein synthesis in old rats. Clin Nutr 2011;30:799–806

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