| First Author | Tao X | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 511 |
| Issue | 1 | Pages | 73-78 |
| PubMed ID | 30770098 | Mgi Jnum | J:290432 |
| Mgi Id | MGI:6442314 | Doi | 10.1016/j.bbrc.2019.02.037 |
| Citation | Tao X, et al. (2019) Genetic deletion of beta2 adrenergic receptors exacerbates hepatocellular lipid accumulation in high-fat diet mice. Biochem Biophys Res Commun 511(1):73-78 |
| abstractText | beta2 Adrenergic receptors (beta2ARs) are G protein-coupled receptors (GPCRs) that are expressed in major insulin target tissues. beta2ARs play an important role in the regulation of lipid metabolism during aging; however, little is known about the significance of beta2ARs in the pathogenesis of hepatic fat accumulation in high-fat diet (HFD) mice. This study aims to examine the role of beta2AR in the development of nonalcoholic fatty liver disease (NAFLD) induced by HFD and the underlying mechanisms. Surprisingly, we found that genetic deletion of beta2AR significantly increased the liver weight of mice fed a HFD for 20 weeks compared to that of wild-type (WT) mice. Moreover, genetic deletion of beta2AR could aggravate HFD-induced liver lipid accumulation and liver injury in mice. Mechanistically, we demonstrated that beta2AR deletion significantly activated PPARgamma/CD36 signaling via inactivation of the cAMP response element-binding (CREB) protein to facilitate hepatocellular lipid deposition in HFD mice. Together, our results identify beta2AR as a plausible therapeutic target for preventing or treating NAFLD. |
