Protein kinase C beta deficiency attenuates obesity syndrome of ob/ob mice by promoting white adipose tissue remodeling

作者：Huang Wei; Bansode Rishipal R; Bal Naresh C; Mehta Madhu; Mehta Kamal D^*

来源：The Journal of Lipid Research, 2012, 53(3): 368-378.

DOI：10.1194/jlr.M019687

• protein kinase C beta
• adipose tissue remodeling
• beta-adrenergic receptors
• thermogenesis

To explore the role of leptin in PKC beta action and to determine the protective potential of PKC beta deficiency on profound obesity, double knockout (DBKO) mice lacking PKC beta 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, PKC beta deficiency increased beta-adrenergic signaling by inducing expression of beta 1- and beta 3-adrenergic receptors (beta-ARs) in white adipose tissue (WAT) of ob/ob mice. Accordingly, p38 MAPK activation and expression of PGC-1 alpha and UCP-1 were increased in WAT of DBKO mice. Consistent with results of in vivo studies, inhibition of PKC beta in WAT explants from ob/ob mice also increased expression of above beta-ARs. In contrast, induction of PGC-1 alpha 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 PKC beta deficiency may prevent genetic obesity, in part, by remodeling the catabolic function of adipose tissues through beta-ARs dependent and independent mechanisms.-Huang, W., R. R. Bansode, N. Bal, M. Mehta, and K. D. Mehta. Protein kinase C beta deficiency attenuates obesity syndrome of ob/ob mice by promoting white adipose tissue remodeling. J. Lipid Res. 2012. 53: 368-378.

• 出版日期2012-3