期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 57, 期 20, 页码 9817-9827出版社
AMER CHEMICAL SOC
DOI: 10.1021/jf902618v
关键词
AMPK; beta cell; EGCG; glucotoxicity; IRS2; Rutin
资金
- National Science council [NSC97-2321-B-002-016]
- National Taiwan University Hospital [NTUH 97-A17]
Pancreatic beta cell failure is one critical metabolic disorder in the development of type 2 diabetes. Decreased viability and dysfunction of beta cells would accelerate the diabetic pathogenesis associated with higher mortality. In this study, the tea polyphenol EGCG (epigallocatechin gallate) and the buckwheat flavonoid Rutin were investigated to attenuate the induced glucotoxicity in beta cells. EGCG and Rutin could preserve the insulin secretory machinery and stimulate insulin receptor substrate 2 (IRS2) signaling in rat pancreatic beta cells, RIN-m5F. These findings further demonstated the reduced glucolipotoxic effects of EGCG and Rutin through activating AMP-activated protein kinase (AMPK) signaling to inhibit the activities of lipogenic enzymes and ameliorating mitochondrial function. Consequently, the cell viability was retained after attenuating the glucotoxicity through the broad effect of EGCG and Rutin. The intrinsic protective effects of EGCG and Rutin in preserving the insulin signaling and regulating lipogenesis, manipulating cell cycling, and maintaining mitochondrial function to achieve the integrity of beta cells, which highlight the possibilities of EGCG and Rutin as novel strategies for the prevention of type 2 diabetes.
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