Abstract
β2 Adrenergic receptors (β2ARs) are G protein-coupled receptors (GPCRs) that are expressed in major insulin target tissues. β2ARs play an important role in the regulation of lipid metabolism during aging; however, little is known about the significance of β2ARs in the pathogenesis of hepatic fat accumulation in high-fat diet (HFD) mice. This study aims to examine the role of β2AR in the development of nonalcoholic fatty liver disease (NAFLD) induced by HFD and the underlying mechanisms. Surprisingly, we found that genetic deletion of β2AR 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 β2AR could aggravate HFD-induced liver lipid accumulation and liver injury in mice. Mechanistically, we demonstrated that β2AR deletion significantly activated PPARγ/CD36 signaling via inactivation of the cAMP response element-binding (CREB) protein to facilitate hepatocellular lipid deposition in HFD mice. Together, our results identify β2AR as a plausible therapeutic target for preventing or treating NAFLD.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
