Benzafibrate induces acyl-CoA oxidase mRNA levels and fatty acid peroxisomal beta-oxidation in rat white adipose tissue

Rats treated with bezafibrate, a PPAR activator, gain less body weight and increase daily food intake. Previously, we have related these changes to a shift of thermogenesis from brown adipose tissue to white adipose tissue at tributable to bezafibrate, which induces uncoupling proteins (UCP), UCP-1 a nd UCP-3, in rat white adipocytes. Nevertheless, UCP induction was weak, im plying additional mechanisms in the change of energy homeostasis produced b y bezafibrate. Here we show that bezafibrate, in addition to inducing UCPs, modifies energy homeostasis by directly inducing aco gene expression and p eroxisomal fatty acid beta -oxidation in white adipose tissue. Further, bez afibrate significantly reduced plasma triglyceride and leptin concentration s, without modifying the levels of PPAR gamma or ob gene in white adipose t issue. These results indicate that bezafibrate reduces the amount of fatty acids available for triglyceride synthesis in white adipose tissue.