| First Author | Huang W | Year | 2012 |
| Journal | J Lipid Res | Volume | 53 |
| Issue | 3 | Pages | 368-78 |
| PubMed ID | 22210924 | Mgi Jnum | J:183125 |
| Mgi Id | MGI:5317509 | Doi | 10.1194/jlr.M019687 |
| Citation | Huang W, et al. (2012) Protein kinase Cbeta deficiency attenuates obesity syndrome of ob/ob mice by promoting white adipose tissue remodeling. J Lipid Res 53(3):368-78 |
| abstractText | To explore the role of leptin in PKCbeta action and to determine the protective potential of PKCbeta deficiency on profound obesity, double knockout (DBKO) mice lacking PKCbeta and ob genes were created, and key parameters of metabolism and body composition were studied. DBKO mice had similar caloric intake as ob/ob mice but showed significantly reduced body fat content, improved glucose metabolism, and elevated body temperature. DBKO mice were resistant to high-fat diet-induced obesity. Moreover, PKCbeta deficiency increased beta-adrenergic signaling by inducing expression of beta1- and beta3-adrenergic receptors (beta-ARs) in white adipose tissue (WAT) of ob/ob mice. Accordingly, p38(MAPK) activation and expression of PGC-1alpha and UCP-1 were increased in WAT of DBKO mice. Consistent with results of in vivo studies, inhibition of PKCbeta in WAT explants from ob/ob mice also increased expression of above beta-ARs. In contrast, induction of PGC-1alpha and UCP-1 expression in brown adipose tissue of DBKO mice was not accompanied by changes in the expression of these beta-ARs. Collectively, these findings suggest that PKCbeta deficiency may prevent genetic obesity, in part, by remodeling the catabolic function of adipose tissues through beta-ARs dependent and independent mechanisms. |
