Dietary oxidized frying oil causes oxidative damage of pancreatic islets and impairment of insulin secretion, effects associated with vitamin E deficiency

doi:10.1017/S0007114510005039

CNU IR > Pharmacy and Science > Dept. of Health and Nutrition (including master's program) > Periodical Articles > Item 310902800/25223

Please use this identifier to cite or link to this item: https://ir.cnu.edu.tw/handle/310902800/25223

Title:	Dietary oxidized frying oil causes oxidative damage of pancreatic islets and impairment of insulin secretion, effects associated with vitamin E deficiency
Authors:	Ya-Fan Chiang Huey-Mei Shaw Mei-Fang Yang Chih-Yang Huang Cheng-Hsien Hsieh Pei-Min Chao
Contributors:	保健營養系
Keywords:	Oxidised frying oil Glucose-stimulated insulin secretion Vitamin E Pancreatic and duodenal homeobox factor-1 c-Jun NH2-terminal kinase
Date:	2011-05
Issue Date:	2012-05-21 16:30:02 (UTC+8)
Abstract:	We previously reported that, in rodents, a diet with a high oxidised frying oil (OFO) content leads to glucose intolerance associated with a reduction in insulin secretion. The present study aimed at investigating the impairment of pancreatic islets caused by dietary OFO. C57BL/6J mice were divided into three groups to receive a low-fat basal diet containing 5 g/100 g of fresh soyabean oil (LF group) or a high-fat diet containing 20 g/100 g of either fresh soyabean oil (HF group) or OFO (HO group). After 8 weeks, mice in the HO group showed glucose intolerance and hypoinsulinaemia, and their islets showed impaired glucose-stimulated insulin secretion (P < 0·05; HO group v. LF and HF groups). Significantly higher oxidative stress and a lower mitochondrial membrane potential were observed in the islets in the HO group compared with the LF and HF groups. Immunoblots showed that the reduction in insulin levels in HO islets was associated with activation of the c-Jun NH2-terminal kinase and a reduction in levels of pancreatic and duodenal homeobox factor-1. In a second study, when dietary OFO-induced tissue vitamin E depletion was prevented by large-dose vitamin E supplementation (500 IU(1·06 mmol all-rac-α-tocopherol acetate)/kg diet; HO+E group), the OFO-mediated reduction in islet size and impairment of glucose tolerance and insulin secretion were significantly attenuated (P < 0·05; HO group v. HO+E group). We conclude that a high level of dietary OFO ingestion impairs glucose metabolism by causing oxidative damage and compromising insulin secretion in pancreatic islets, and that these effects can be prevented by vitamin E supplementation.
Relation:	British Journal of Nutrition 105(9)：p.1311-1319
Appears in Collections:	[Dept. of Health and Nutrition (including master's program)] Periodical Articles

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