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首页> 外文期刊>Diabetes/metabolism research and reviews >Mitochondrial dysfunction as a central event for mechanisms underlying insulin resistance: the roles of long chain fatty acids.
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Mitochondrial dysfunction as a central event for mechanisms underlying insulin resistance: the roles of long chain fatty acids.

机译:线粒体功能障碍是潜在的胰岛素抵抗机制的中心事件:长链脂肪酸的作用。

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Insulin resistance is characterized by hyperglycaemia, dyslipidaemia and oxidative stress prior to the development of type 2 diabetes mellitus. To date, a number of mechanisms have been proposed to link these syndromes together, but it remains unclear what the unifying condition that triggered these events in the progression of this metabolic disease. There have been a steady accumulation of data in numerous experimental studies showing the strong correlations between mitochondrial dysfunction, oxidative stress and insulin resistance. In addition, a growing number of studies suggest that the raised plasma free fatty acid level induced insulin resistance with the significant alteration of oxidative metabolism in various target tissues such as skeletal muscle, liver and adipose tissue. In this review, we herein propose the idea of long chain fatty acid-induced mitochondrial dysfunctions as one of the key events in the pathophysiological development of insulin resistance and type 2 diabetes. The accumulation of reactive oxygen species, lipotoxicity, inflammation-induced endoplasmic reticulum stress and alterations of mitochondrial gene subset expressions are the most detrimental that lead to the developments of aberrant intracellular insulin signalling activity in a number of peripheral tissues, thereby leading to insulin resistance and type 2 diabetes.
机译:在2型糖尿病发生之前,胰岛素抵抗的特征是高血糖,血脂异常和氧化应激。迄今为止,已经提出了许多机制将这些综合症联系在一起,但是目前尚不清楚在这种代谢性疾病的发展过程中触发这些事件的统一条件是什么。大量的实验研究已经积累了稳定的数据,这些研究表明线粒体功能障碍,氧化应激和胰岛素抵抗之间存在很强的相关性。此外,越来越多的研究表明,血浆游离脂肪酸水平的升高会诱导胰岛素抵抗,并在骨骼肌,肝脏和脂肪组织等各种靶组织中引起氧化代谢的显着改变。在本文中,我们提出了长链脂肪酸诱导的线粒体功能障碍的想法,将其作为胰岛素抵抗和2型糖尿病的病理生理发展中的关键事件之一。活性氧的积累,脂毒性,炎症引起的内质网应激和线粒体基因亚群表达的改变是最有害的,导致许多周围组织细胞内胰岛素信号转导活性异常发展,从而导致胰岛素抵抗和2型糖尿病。

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