作者: Jill M. Schroeder-Gloeckler , Shaikh Mizanoor Rahman , Rachel C. Janssen , Liping Qiao , Jianhua Shao
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摘要: CCAAT/enhancer-binding protein beta (C/EBPbeta) plays a key role in initiation of adipogenesis adipose tissue and gluconeogenesis liver; however, the C/EBPbeta hepatic lipogenesis remains undefined. Here we show that inactivation Lepr(db/db) mice attenuates obesity, fatty liver, diabetes. In addition to impaired adipogenesis, livers from C/EBPbeta(-/-) x had dramatically decreased triglyceride content reduced lipogenic enzyme activity. deletion down-regulated peroxisome proliferator-activated receptor gamma2 (PPARgamma2) stearoyl-CoA desaturase-1 up-regulated PPARalpha independent SREBP1c. Conversely, overexpression wild-type increased PPARgamma2 mRNA content. FAO cells, liver inhibiting form or RNA interference attenuated palmitate-induced accumulation levels vivo. Leptin anti-diabetic drug metformin acutely expression hepatocytes, whereas acids up-regulate expression. These data provide novel evidence linking energy balance with important implications for treatment obesity disease.