Pparg increases the transcription of Srebf1, which activates other adipogenic genes and promotes the conversion of pyruvate to fatty acids.[57] Conversely, hepatocyte‐specific knockout of Pparg in leptin‐deficient mice ameliorated hepatic steatosis and exacerbated diabetic phenotypes.[58] Several Pparg antagonists have also been reported to mitigate hyperglycemia and hyperinsulinemia and to reduce the plasma levels of Tnf in ob/ob mice.[59] Taken together, the proadipogenic influence of Pparg in the liver exacerbates hepatic lipid accumulation and worsens IR. This evidence concerns the gene SREBF1 and hyperinsulinism.