Objective: To investigate the effect of peroxisome proliferation activated receptor-α(PPAR-α)activator on the fatty acid
oxidation and the molecular mechanisms to improve high fat induced
insulin resistance. Methods: Male SD rats were divided into 3 groups, group A (n=10): rats fed with saturated fatty acid, group B (n=10): rats fed with unsaturated fatty acid, group C (n=10): control rats. At the end of 4th weeks, the first 2 groups were divided into two groups: rats with or without Bezafibrate treatment. After another two weeks, blood samples were taken to detect fasting plasma glucose (FPG), fasting plasma insulin (FIN) and triglyceride (TG). The muscle, hepatic liver and adipose tissues were taken out from all the rats to assay the expression of PPAR-αand musle-type carnitine palmitoyltranferanse-1(CPT-1) mRNA by RT-PCR. Results: The expression of CPT-1 mRNA of musle and adipose tissues in no Bezafibrate treatment groups was lower than the Bezafibrate treatment groups and control but the expression of PPAR-αmRNA had no significant difference among all groups. Conclusions: The expression of CPT-1 mRNA is significantly decreased in high fat fed rats. PPAR-α activator bezafibrate can increase the expression of CPT-1. PPAR-α mRNA has no change in every group, suggesting that high fatty acid can suppress fatty acid
β-oxidation and cause lipid accumulation and insulin resistance. PPAR-α activator can attenuate insulin resistance by increase fatty acid β-oxidation. This effect is not through suppress or promote the transcription of PPAR-α but as ligand to regulate fatty acid oxidation.