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高血糖诱导的肝脏线粒体改变。

Hyperglycemia-induced mitochondrial alterations in liver.

机构信息

Life Science Division, AU-KBC Research Centre, MIT Campus of Anna University, Chromepet, Chennai, India.

出版信息

Life Sci. 2010 Aug 14;87(7-8):197-214. doi: 10.1016/j.lfs.2010.06.007. Epub 2010 Jun 17.

DOI:10.1016/j.lfs.2010.06.007
PMID:20600152
Abstract

The increasing prevalence of diabetes continues to be a major health issue world wide. Liver injury is highly relevant in diabetic subjects and Type 2 diabetes mellitus is an acknowledged risk factor for non-alcoholic fatty liver disease (NAFLD). Chronic hyperglycemia is an important feature of diabetes and hyperglycemia induced mitochondrial dysfunction in liver holds importance in context to NAFLD. Some of the hyperglycemia induced changes in mitochondria include decreased oxidative phosphorylation, increased oxidative stress and ultra structural abnormalities. The following review identifies the mechanisms through which hyperglycemia causes mitochondrial dysfunction in liver.

摘要

糖尿病的患病率不断上升,仍然是全球范围内的一个主要健康问题。肝脏损伤与糖尿病患者密切相关,2 型糖尿病是非酒精性脂肪性肝病(NAFLD)的公认危险因素。慢性高血糖是糖尿病的一个重要特征,高血糖诱导的肝脏线粒体功能障碍在 NAFLD 中具有重要意义。高血糖引起的线粒体变化包括氧化磷酸化减少、氧化应激增加和超微结构异常。以下综述确定了高血糖导致肝脏线粒体功能障碍的机制。

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