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The role of uncoupling protein 2 in the development of type 2 diabetes.

机译:解偶联蛋白2在2型糖尿病发育中的作用。

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Uncoupling proteins (UCP) are carriers expressed in the mitochondrial inner membrane that uncouple oxygen consumption by the respiratory chain from ATP synthesis. UCP2 is a member of the multigenic UCP family that is expressed in a wide range of tissues and organs. Possible functions of UCP2 include control of ATP synthesis, regulation of fatty acid metabolism and control of reactive oxygen species production. UCP2 expression in tissues involved in lipid and energy metabolism and mapping of the gene to a region linked to obesity and hyperinsulinemia prompted studies on the involvement of UCP2 in metabolic disorders, and especially in type 2 diabetes. In human adipose tissue and skeletal muscle, UCP2 expression is increased during fasting. The carrier was shown to be under the control of fatty acids and thyroid hormones in vivo. An upregulation has been observed in the liver during high-fat feeding and obesity. However, data in UCP2 gene knockout mice do not support a role for UCP2 in steatohepatitis. The most compelling metabolic role of UCP2 comes from studies in pancreatic beta cells. Overexpression in isolated pancreatic islets results in decreased ATP content and blunted glucose-stimulated insulin secretion. UCP2-deficient mice show an increased ATP level and an enhanced insulin secretion. Lack of UCP2 dramatically improves insulin secretion and decreases hyperglycemia in leptin-deficient mice. The role of UCP2 in the control of insulin secretion constitutes, to date, the most pertinent path to investigate in a therapeutic perspective. (c) 2003 Prous Science. All rights reserved.
机译:非偶像蛋白(UCP)是在线粒体内膜中表达的载体,其通过来自ATP合成的呼吸链不稳定氧消耗。 UCP2是多群UCP系列的成员,其在各种组织和器官中表达。 UCP2的可能功能包括控制ATP合成,调节脂肪酸代谢和反应性氧物种生产的控制。在脂质和能量代谢的组织中的UCP2表达和基因的映射到与肥胖和高胰岛素血症相关的区域,促使UCP2在代谢紊乱中的参与研究,特别是在2型糖尿病中。在人脂肪组织和骨骼肌中,在禁食期间增加了UCP2表达。载体显示在体内脂肪酸和甲状腺激素的控制下。在高脂肪喂养和肥胖期间,肝脏中观察到上调。然而,UCP2基因敲除小鼠的数据不支持UCP2在胫骨肝炎中的作用。 UCP2最引人注目的代谢作用来自胰腺β细胞中的研究。分离的胰岛含量的过度表达导致ATP含量下降和钝化葡萄糖刺激的胰岛素分泌。 UCP2缺陷小鼠显示ATP水平增加和增强的胰岛素分泌。缺乏UCP2显着改善了胰岛素分泌,并降低了瘦素缺乏小鼠的高血糖。 UCP2在胰岛素分泌控制中的作用迄今为止,迄今为止,迄今为止以治疗性的观点进行研究。 (c)2003年律师科学。版权所有。

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