it is believed to be involved in the upregulation of PDK4 in response to fasting [40]. The essential role of PPARα in the induction of PDK4 upon fasting was also confirmed by the absence of this response in PPARα knockout mice [39]. Furthermore, in wild-type mice, PDK4 levels were normalized after 6 hours refeeding following a period of fasting, which caused suppression of gluconeogenic rates and stimulation of glycolysis and lipogenesis. This response was blunted as well in PPARα −/− mice [39].
