Disruption of mitochondria-associated ER membranes impairs insulin sensitivity and thermogenic function of adipocytes.

ABSTRACT: The prevalence and healthcare burden of obesity and its related metabolic disorders such as type 2 diabetes (T2D) are increasing rapidly. A better understanding of the pathogenesis of these diseases helps to find the therapeutic strategies. Mitochondria and endoplasmic reticulum (ER) are two important organelles involved in the maintenance of intracellular Ca²⁺ and ROS homeostasis. Their functional defects are thought to participate in the pathogenesis of insulin resistance or T2D. The proper structure and function of the mitochondria-associated ER membranes (MAMs) is required for efficient communication between the ER and mitochondria and defects in MAMs have been shown to play a role in metabolic syndrome and other diseases. However, the detailed mechanism to link MAMs dysfunc

SUBMITTER: Wang CH 

PROVIDER: S-EPMC9504280 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature