TAILIEUCHUNG - Báo cáo khoa học: Suppression of NADPH oxidase 2 substantially restores glucose-induced dysfunction of pancreatic NIT-1 cells

Defects in insulin secretion by pancreatic cells and⁄or decreased sensitivity of target tissues to insulin action are the key features of type 2 diabetes. It has been shown that excessive generation of reactive oxygen species (ROS) is linked to glucose-induced b-cell dysfunction. | 1FEBS Journal Suppression of NADPH oxidase 2 substantially restores glucose-induced dysfunction of pancreatic NIT-1 cells Huiping Yuan Yonggang Lu Xiuqing Huang Qinghua He Yong Man Yingsheng Zhou Shu Wang and Jian Li Peking University Fifth Schoolof ClinicalMedicine Beijing Hospital Beijing China Keywords apoptosis glucose NADPH oxidase 2 NIT-1 cells reactive oxygen species Correspondence J. Li Peking University Fifth Schoolof Clinical Medicine Beijing Hospital Beijing 100730 China Fax 86 10 65237929 Tel 86 10 58115048 E-mail lijian@ Received 2 August 2010 revised 28 September 2010 accepted 11 October 2010 doi Defects in insulin secretion by pancreatic cells and or decreased sensitivity of target tissues to insulin action are the key features of type 2 diabetes. It has been shown that excessive generation of reactive oxygen species ROS is linked to glucose-induced b-cell dysfunction. However cellular mechanisms involved in ROS generation in b-cells and the link between ROS and glucose-induced b-cell dysfunction are poorly understood. Here we demonstrate a key role of NADPH oxidase 2 NOX2 -derived ROS in the deterioration of b-cell function induced by a high concentration of glucose. Sprague-Dawley rats were fed a high-fat diet for 24 weeks to induce diabetes. Diabetic rats showed increased glucose levels and elevated ROS generation in blood but decreased insulin content in pancreatic b-cells. In vitro increased ROS levels in pancreatic NIT-1 cells exposed to high concentrations of glucose mmol L-1 were associated with elevated expression of NOX2. Importantly decreased glucose-induced insulin expression and secretion in NIT-1 cells could be rescued via siRNA-mediated NOX2 reduction. Furthermore high glucose concentrations led to apoptosis of b-cells by activation of p38MAPK and p53 and dysfunction of b-cells through phosphatase and tensih homolog PTEN -dependent Jun N-termi-nal kinase JNK activation and protein kinase B

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