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Genetic deletion of β 2 adrenergic receptors exacerbates hepatocellular lipid accumulation in high-fat diet mice.
Biochemical and Biophysical Research Communications 2019 Februrary 13
β2 Adrenergic receptors (β2 ARs) are G protein-coupled receptors (GPCRs) that are expressed in major insulin target tissues. β2 ARs play an important role in the regulation of lipid metabolism during aging; however, little is known about the significance of β2 ARs in the pathogenesis of hepatic fat accumulation in high-fat diet (HFD) mice. This study aims to examine the role of β2 AR in the development of nonalcoholic fatty liver disease (NAFLD) induced by HFD and the underlying mechanisms. Surprisingly, we found that genetic deletion of β2 AR 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 β2 AR could aggravate HFD-induced liver lipid accumulation and liver injury in mice. Mechanistically, we demonstrated that β2 AR 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 β2 AR as a plausible therapeutic target for preventing or treating NAFLD.
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