Xlab, Center for Healthy Aging, Faculty of Medicine, University of Copenhagen, Denmark.
Int J Biochem Cell Biol. 2013 Jan;45(1):11-5. doi: 10.1016/j.biocel.2012.09.019. Epub 2012 Oct 2.
The mechanism(s) behind the decreased ability of insulin to facilitate glucose uptake in insulin sensitive tissues as seen in type 2 diabetes is not resolved. With the rapidly increasing prevalence of this disease world-wide, and the many complications that follow the disease, large resources are used in the attempt to resolve the mechanisms of insulin resistance. In this context, a dysfunction of mitochondria in the skeletal muscle has been suggested to play a pivotal role. It has been postulated that a decrease in the content of mitochondria in the skeletal muscle can explain the insulin resistance. Complementary to this also specific defects of components in the respiratory chain in the mitochondria have been suggested to play a role in insulin resistance. A key element in these mechanistic suggestions is inability to handle substrate fluxes and subsequently an accumulation of ectopic intramyocellular lipids, interfering with insulin signaling. In this review we will present the prevailing view-points and argue for the unlikelihood of this scenario being instrumental in human insulin resistance. This article is part of a Directed Issue entitled: Bioenergetic dysfunction.
在 2 型糖尿病中，胰岛素促进胰岛素敏感组织摄取葡萄糖的能力下降的机制尚未得到解决。随着这种疾病在全球范围内的迅速流行，以及随之而来的许多并发症，人们投入了大量资源来试图阐明胰岛素抵抗的机制。在这种情况下，有人提出，骨骼肌中线粒体的功能障碍可能起着关键作用。有人推测，骨骼肌中线粒体的含量减少可以解释胰岛素抵抗。与之互补的是，线粒体呼吸链中特定成分的缺陷也被认为在胰岛素抵抗中起作用。这些机制假设的一个关键因素是无法处理底物通量，随后会积累异位肌内脂质，干扰胰岛素信号。在这篇综述中，我们将介绍目前的观点，并认为这种情况不太可能是导致人类胰岛素抵抗的原因。本文是题为“生物能量功能障碍”的专题的一部分。
