Gutiérrez-Rodelo Citlaly, Roura-Guiberna Adriana, Olivares-Reyes Jesús Alberto
Laboratorio de Transducción de Señales, Departamento de Bioquímica, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (IPN), Ciudad de México, México.
Gac Med Mex. 2017 Mar-Apr;153(2):214-228.
The biological actions of insulin are initiated by activating its membrane receptor, which triggers multiple signaling pathways to mediate their biological actions. Due to the importance of metabolic regulation and promoting functions of cell growth and proliferation, insulin actions are highly regulated to promote proper metabolic functioning and energy balance. If these mechanisms are altered, this can lead to a condition known as insulin resistance, which is the consequence of a deficient insulin signaling caused by mutations or post-translational modifications of the receptor or effector molecules located downstream. Insulin resistance is one of the main characteristics of pathological manifestations associated with type 2 diabetes mellitus, one of the leading causes of death in Mexico and worldwide. In recent years, it has been found that conditions such as inflammation, endoplasmic reticulum stress, and mitochondrial dysfunction promote insulin resistance. The aim of this review is to elucidate the molecular aspects of insulin resistance and the mechanisms involved in regulating its effects, with particular emphasis on the role of inflammation, endoplasmic reticulum stress, and mitochondrial dysfunction.
胰岛素的生物学作用通过激活其膜受体而启动,该受体触发多种信号通路来介导其生物学作用。由于代谢调节以及促进细胞生长和增殖功能的重要性,胰岛素的作用受到高度调节,以促进正常的代谢功能和能量平衡。如果这些机制发生改变,可能会导致一种称为胰岛素抵抗的病症,这是由位于下游的受体或效应分子的突变或翻译后修饰引起的胰岛素信号传导不足的结果。胰岛素抵抗是与2型糖尿病相关的病理表现的主要特征之一,2型糖尿病是墨西哥和全球主要的死亡原因之一。近年来,已发现诸如炎症、内质网应激和线粒体功能障碍等情况会促进胰岛素抵抗。本综述的目的是阐明胰岛素抵抗的分子方面以及调节其作用的机制,特别强调炎症、内质网应激和线粒体功能障碍的作用。