Treatment of mice with fenofibrate resulted in increased expression of glycerol kinase [30]. Fasting as well as treatment with WY14643 induced an upregulation of the expression of genes involved in hepatic gluconeogenesis from glycerol, including AQP3, AQP9, cGDPH, mGDPH, and glycerol kinase [22], which was dependent on the presence of PPARα (Figure 2). In line with the upregulation of glycerol utilization genes via PPARα, WY14643 significantly decreased plasma glycerol levels in wild type but not in PPARα −/− mice [22]. This decrease in plasma glycerol levels was also observed in human atherosclerotic patients treated with fenofibrate for 4 weeks [22].
