More consistent results were obtained in studies where a prolonged period of fasting was followed by refeeding. Repletion of glycogen stores via hepatic glycogen synthesis was consistently impaired by PPARα deficiency in all studies [20, 39, 44], despite normal insulin and glucose levels after refeeding [39]. It was proposed to be the consequence of reduced FAO and subsequently reduced gluconeogenesis and glycogen synthesis due to hampered production of substrates [39]. In the absence of PPARα, expression of Gys-2 was markedly reduced during refeeding after prolonged fasting [44], likely explaining the diminished rate of glycogen formation upon refeeding in PPARα −/− mice.
