Obesity and insulin resistance (IR) are associated with endoplasmic reticulum (ER) stress and mitochondrial dysfunction in several tissues. Although for many years mitochondrial and ER function were studied separately, these organelles also connect to produce interdependent functions. Communication occurs at mitochondria-associated ER membranes (MAM) and regulates lipid and calcium homeostasis, apoptosis, and the exchange of adenine nucleotides, among other things. Recent evidence suggests that MAMs contribute to organelle, cellular, and systemic metabolism. In obesity and IR models, metabolic tissues such as the liver, skeletal muscle, pancreas, and adipose tissue present alterations in MAM structure or function. The purpose of this mini-review is to highlight the MAM disruptions that occur in each tissue during obesity and IR and its relationship with glucose homeostasis and IR. We also discuss the current controversy that surrounds MAMs' role in the development of insulin resistance.

中文翻译：

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线粒体相关的ER膜在葡萄糖稳态和胰岛素抵抗中的作用。

肥胖和胰岛素抵抗（IR）与某些组织的内质网（ER）应激和线粒体功能障碍有关。尽管多年来分别研究了线粒体和内质网功能，但这些细胞器也相互连接以产生相互依赖的功能。通讯发生在与线粒体相关的ER膜（MAM）上，并调节脂质和钙的体内稳态，细胞凋亡和腺嘌呤核苷酸的交换等。最近的证据表明，MAM有助于细胞器，细胞和全身代谢。在肥胖症和IR模型中，代谢组织（例如肝脏，骨骼肌，胰腺和脂肪组织）的MAM结构或功能发生改变。这次迷你回顾的目的是强调肥胖和IR期间每个组织中发生的MAM破坏及其与葡萄糖稳态和IR的关系。我们还讨论了围绕MAM在胰岛素抵抗发展中作用的当前争议。