| First Author | Wang L | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 429 |
| Issue | 1-2 | Pages | 99-104 |
| PubMed ID | 23111327 | Mgi Jnum | J:191093 |
| Mgi Id | MGI:5460943 | Doi | 10.1016/j.bbrc.2012.10.077 |
| Citation | Wang L, et al. (2012) GRK5 ablation contributes to insulin resistance. Biochem Biophys Res Commun 429(1-2):99-104 |
| abstractText | The G-protein-coupled receptor kinase 5 (GRK5) is an important member of the threonine/serine kinase family that phosphorylates and regulates the G-protein-coupled receptor (GPCR) signaling pathway. GRK5 is highly expressed in adipose tissue and may act as an adipogenetic factor under high-fat load [1]. Insulin resistance is associated with the pathogenesis of metabolic disorders such as type 2 diabetes and obesity; however, the potential role of GRK5 in insulin resistance is unknown. We characterized the biochemical and molecular alterations related to metabolic complications observed in GRK5(-/-) mice. These mice, which are partially resistant to obesity induced by a high-fat diet, had impaired glucose tolerance and insulin sensitivity, as well as disruption of AKT signaling transduction compared with their wild-type littermates. Further study showed that the decreased insulin sensitivity was not attributable to alterations in inflammatory status such as the NF-kappaB signaling pathway or inflammatory gene expression. Instead, hepatic steatosis and changes of mRNA in genes involved in hepatic glucose and lipid homeostasis were found. Overall, our data identified GRK5 as a positive regulator of insulin sensitivity. Our results showed that this protein is a potential therapeutic target in the treatment of insulin resistance and related disorders. |
