Endothelial APLNR regulates tissue fatty acid uptake and is essential for apelin's glucose-lowering effects.

ABSTRACT: Treatment of type 2 diabetes mellitus continues to pose an important clinical challenge, with most existing therapies lacking demonstrable ability to improve cardiovascular outcomes. The atheroprotective peptide apelin (APLN) enhances glucose utilization and improves insulin sensitivity. However, the mechanism of these effects remains poorly defined. We demonstrate that the expression of APLNR (APJ/AGTRL1), the only known receptor for apelin, is predominantly restricted to the endothelial cells (ECs) of multiple adult metabolic organs, including skeletal muscle and adipose tissue. Conditional endothelial-specific deletion of Aplnr (Aplnr^ECKO ) resulted in markedly impaired glucose utilization and abrogation of apelin-induced glucose lowering. Furthermore, we

SUBMITTER: Hwangbo C 

PROVIDER: S-EPMC5703224 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature