Mitochondria-associated ER membranes in glucose homeostasis and insulin resistance.
Logan K TownsendHenver S BrunettaMarcelo A S MoriPublished in: American journal of physiology. Endocrinology and metabolism (2020)
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 (MAMs) 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 IR.
Keyphrases
- insulin resistance
- endoplasmic reticulum
- adipose tissue
- skeletal muscle
- high fat diet induced
- metabolic syndrome
- high fat diet
- polycystic ovary syndrome
- type diabetes
- oxidative stress
- gene expression
- weight loss
- blood glucose
- endoplasmic reticulum stress
- estrogen receptor
- breast cancer cells
- weight gain
- cell cycle arrest
- blood pressure
- cell proliferation
- body mass index
- reactive oxygen species
- pi k akt