Endothelial ERα promotes glucose tolerance by enhancing endothelial insulin transport to skeletal muscle.

ABSTRACT: The estrogen receptor (ER) designated ERα has actions in many cell and tissue types that impact glucose homeostasis. It is unknown if these include mechanisms in endothelial cells, which have the potential to influence relative obesity, and processes in adipose tissue and skeletal muscle that impact glucose control. Here we show that independent of impact on events in adipose tissue, endothelial ERα promotes glucose tolerance by enhancing endothelial insulin transport to skeletal muscle. Endothelial ERα-deficient male mice are glucose intolerant and insulin resistant, and in females the antidiabetogenic actions of estradiol (E2) are absent. The glucose dysregulation is due to impaired skeletal muscle glucose disposal that results from attenuated muscle insulin delivery. Endothelial ERα act

SUBMITTER: Sacharidou A 

PROVIDER: S-EPMC10435471 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature