Depending on the nutritional status, the importance of glycerol as gluconeogenic precursor varies from 5% postprandial in humans to being the main gluconeogenic precursor after prolonged starvation in rodents [22]. Inasmuch as the conversion of glycerol to glucose in liver is impaired in PPARα −/− mice, defective synthesis of glucose from glycerol may partly explain the fasting-induced hypoglycemia in PPARα −/− mice. In conclusion, the metabolic fate of glycerol is under the control of PPARα, which stimulates its conversion to glucose in liver (Figure 2).
