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Endogenous regulation of insulin secretion by UCP2.

作者信息

Chan Catherine B

机构信息

Department of Anatomy & Physiology, University of Prince Edward Island, Charlottetown, PE Canada.

出版信息

Clin Lab. 2002;48(11-12):599-604.

PMID:12465744
Abstract

Uncoupling protein 2 (UCP2) expression is more-or-less ubiquitous, in tissues of diverse function. Its presence in adipose and muscle is postulated to be involved in regulation of energy expenditure and nutrient partitioning, particularly that of fats. In pancreatic islet beta cells, induction of UCP2 is shown to inhibit glucose-stimulated insulin secretion. Thus, insufficient insulin secretion in models of type 2 diabetes is associated with elevated UCP2 expression in islets. The evidence for such a role for UCP2 in the regulation of insulin secretion in islets is reviewed.

摘要

相似文献

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Uncoupling protein 2 and islet function.解偶联蛋白2与胰岛功能
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Uncoupling protein-2 negatively regulates insulin secretion and is a major link between obesity, beta cell dysfunction, and type 2 diabetes.解偶联蛋白-2对胰岛素分泌起负调节作用,是肥胖、β细胞功能障碍与2型糖尿病之间的主要关联因素。
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UCP2 mRNA expression is dependent on glucose metabolism in pancreatic islets.UCP2 mRNA 的表达依赖于胰岛中的葡萄糖代谢。
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Free fatty acid-induced beta-cell defects are dependent on uncoupling protein 2 expression.游离脂肪酸诱导的β细胞缺陷依赖于解偶联蛋白2的表达。
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Uncoupling protein-2 mediates the protective action of berberine against oxidative stress in rat insulinoma INS-1E cells and in diabetic mouse islets.解偶联蛋白2介导小檗碱对大鼠胰岛素瘤INS-1E细胞和糖尿病小鼠胰岛氧化应激的保护作用。
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The uncoupling protein 1 gene, UCP1, is expressed in mammalian islet cells and associated with acute insulin response to glucose in African American families from the IRAS Family Study.解偶联蛋白1基因(UCP1)在哺乳动物胰岛细胞中表达,并且在胰岛素抵抗动脉粥样硬化研究(IRAS)家族研究中的非裔美国家庭中,与对葡萄糖的急性胰岛素反应相关。
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