Whole-body Pparα−/− mice show impaired coping with prolonged fasting, resulting in defective fatty acid oxidation and steatosis, hypoglycaemia and hypothermia. However, PPARα also contributes to metabolic homeostasis through expression in other tissues. Here we investigated the impact of hepatocyte-specific PPARα deletion on liver physiology and lipid metabolism in vivo. To our knowledge, this is the first report that selective PPARα deletion in hepatocytes (Pparαhep−/−) was sufficient to promote hepatic steatosis.
