Hepatic GRK2 is dispensable for glucose homeostasis and other key metabolic parameters in mice.

ABSTRACT:

Objective

G-protein-coupled receptor (GPCR) kinases (GRKs) abrogate GPCR signaling by promoting receptor desensitization and internalization. Accumulating evidence suggests that GRK2 represents an important regulator of GPCR-mediated effects on systemic glucose metabolism, obesity, and insulin resistance. Despite the key role of the liver in maintaining euglycemia, the potential metabolic relevance of hepatic GRK2 has yet to be examined. Thus, the goal of this study was to explore the potential role of hepatic GRK2 in maintaining glucose homeostasis and other key metabolic functions.

Methods

To address this question, we generated mice that showed a ∼90% reduction in GRK2 protein expression selectively in hepatocytes (Hep-GRK2-KO mice) and subjected these mice, together with

SUBMITTER: Oteng AB 

PROVIDER: S-EPMC10809122 | biostudies-literature | 2024 Jan

REPOSITORIES: biostudies-literature