Hôpital Robert Debré, Paris, France.
Université Paris 7, Faculté de médecine Denis Diderot, IFR02, Paris, France.
J Inherit Metab Dis. 2009 Dec;32(6):684-698. doi: 10.1007/s10545-009-1263-0. Epub 2009 Oct 11.
Diabetes mellitus is occasionally observed in patients with skeletal muscle respiratory chain deficiency, suggesting that skeletal muscle mitochondrial dysfunction might play a pathogenic role in type 2 diabetes (T2D). In support of this hypothesis, decreased muscle mitochondrial activity has been reported in T2D patients and in mouse models of diabetes. However, recent work by several groups suggests that decreased muscle mitochondrial function may be a consequence rather than a cause of diabetes, since decreased mitochondrial function in mice affords protection from diabetes and obesity. We review the data on this controversial but important issue of potential links between mitochondrial dysfunction and diabetes.
糖尿病在骨骼肌呼吸链缺陷的患者中偶尔会被观察到，这表明骨骼肌线粒体功能障碍可能在 2 型糖尿病（T2D）中发挥致病作用。支持这一假说，T2D 患者和糖尿病小鼠模型中均报道了肌肉线粒体活性的降低。然而，最近几个研究小组的工作表明，肌肉线粒体功能的降低可能是糖尿病的结果而不是原因，因为小鼠中线粒体功能的降低提供了对糖尿病和肥胖的保护。我们回顾了关于线粒体功能障碍与糖尿病之间潜在联系的这一有争议但重要的问题的数据。
