From the above, it appears that hepatic PPARα plays an important role in carbohydrate handling in rodent liver by regulating expression of genes in a direct or indirect way. During the fed to fasting transition, PPARα activation contributes to the inhibition of glycolysis and to the induction of gluconeogenesis. However, since only a few genes were shown to be directly targeted by PPARα, these effects are mostly governed by indirect mechanisms that remain to be clarified. Together with its well-known stimulatory effect on β-oxidation, a switch occurs from glucose to FA as the primary fuel source. PPARα also impacts on the balance between glycogen synthesis and glycogenolysis. Although PPARα activation is associated with a reduction in glycogen stores, it remains controversial how this is precisely established.
