However, in addition to this increase in MDH activity, our group observed that PPARα KO mice subjected to a HFD had lower gluconeogenesis in pyruvate tolerance test (data not shown), indicating that this excess of Krebs cycle intermediates may be converted to other pathways, such as de novo lipogenesis, as indicated by the higher expression levels of ACC and by the more severe steatosis observed in the KO mice. The gene discussed is MDH2; the disease is steatosis.