MTCH2 Suppresses Thermogenesis by Regulating Autophagy in Adipose Tissue.

ABSTRACT: Stimulating adipose tissue thermogenesis has emerged as a promising strategy for combating obesity, with uncoupling protein 1 (UCP1) playing a central role in this process. However, the mechanisms that suppress adipose thermogenesis and energy dissipation in obesity are not fully understood. This study identifies mitochondrial carrier homolog 2 (MTCH2), an obesity susceptibility gene, as a negative regulator of energy homeostasis across flies, rodents, and humans. Notably, adipose-specific MTCH2 depletion in mice protects against high-fat-diet (HFD)-induced obesity and metabolic disorders. Mechanistically, MTCH2 deficiency promotes energy expenditure by stimulating thermogenesis in brown adipose tissue (BAT) and browning of subcutaneous white adipose tissue (scWAT), accompanied by upregula

SUBMITTER: Zhao XY 

PROVIDER: S-EPMC12061245 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature