P32 heterozygosity protects against age- and diet-induced obesity by increasing energy expenditure.

ABSTRACT: Obesity is increasing in prevalence and has become a global public health problem. The main cause of obesity is a perturbation in energy homeostasis, whereby energy intake exceeds energy expenditure. Although mitochondrial dysfunction has been linked to the deregulation of energy homeostasis, the precise mechanism is poorly understood. Here, we identify mitochondrial p32 (also known as C1QBP) as an important regulator of lipid homeostasis that regulates both aerobic and anaerobic energy metabolism. We show that while whole-body deletion of the p32 results in an embryonic lethal phenotype, mice heterozygous for p32 are resistant to age- and high-fat diet-induced ailments, including obesity, hyperglycemia, and hepatosteatosis. Notably, p32 ^+/- mice are apparently healthy, demonstr

SUBMITTER: Liu Y 

PROVIDER: S-EPMC5516014 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature