摘要：Background: Coconut milk consumption in middle- aged male rats can cause increased blood vessel endothelial nitric oxide synthase (eNOS) and cystathionine- γ- lyase (CSE) protein expression, and decreased fasting blood glucose. Objective: The present study aimed to investigate whether coconut milk oil (CO), the major constituents of the coconut milk, wasresponsible for those effects. Methods: CO was isolated from dried fresh coconut milk and gavaged (1 and 3 ml/kg) to middleaged male rats for 6 weeks. Animal body weight and food intake, internal organ weight, blood biochemistry, lipid profile, basal blood pressure and heart rate and vascular functions were investigated. Results: In comparison to a distilled water control group, no differences were observed in any of the parameters studied in the group fed 1 ml/kg of CO except for an increase in retroperitoneal fat accumulation. Feeding 3 ml/kg of CO caused decreased fasting blood glucose, plasma alkaline phosphatase and blood urea nitrogen and liver cell lipid accumulation, but increased retroperitoneal fat tissue. It also caused decreased maximal contractile response of endotheliumintact thoracic aortic rings to phenylephrine although the effect disappeared in the presence of Nnitro-L-arginine (L-NA) or removal of the endothelium. DL-propargylglycine together with L-NA caused a higher contraction to phenylephrine in the CO-treated groups than in the control group. It also caused an increase in vasodilatation to acetylcholine, but not to glyceryl trinitrate, of the phenylephrine pre-contracted aortic rings. CO treatment caused increased vascular wall eNOS and CSE protein expression. Conclusion: CO at a dose of 3 ml/kg causes some decrease in cardiovascular risk factors in middleaged male rats, although the amount of CO consumption should be limited as it caused an increase in retroperitoneal fat.
