Effect of pineapple on lipid metabolism in high cholesterol diet-fed rats

Abstract

Excessive consumption of a high cholesterol diet (HCD) leads to the development of hepatic steatosis, and dyslipidaemia. Previous studies have showed that many types of fruit are rich in fibre, vitamins, and phytochemicals, which are able to lower lipid levels in the blood and alleviate hepatic steatosis. Pineapples have been reported to exhibit anti-oxidants, anti-toxicity, anti-obesity, and anti-hepatic steatosis activities. The aim of this study was therefore to investigate the effects of powdered pineapple on hyperlipidaemia and hepatic lipid metabolism in the HCD-fed rats. Male Sprague-Dawley rats were divided into four groups: the control group (C) received normal diet, the high cholesterol diet group (HCD) received HCD, the pineapple group (HCD+P) received HCD plus 200 mg/kg body weight of powdered pineapple, and the simvastatin group (HCD+S) received HCD plus 40 mg/kg body weight of simvastatin. After 8 weeks of experiments, the lipid levels in the blood and livers of the rats were measured. The expression of the proteins involved in cholesterol metabolism was determined in the liver tissues by Western blot analysis. Our results showed that the powdered pineapple reduced body, and liver weights, and liver to body weight ratio in the HCD-fed rats. Pineapple-treated hypercholesterolemic rats exhibited significantly reduced serum TC, TG, LDL-c, AST, and ALT levels, as well as decreased hepatic TC and TG contents compared with the HCD group. Daily consumption of powdered pineapple also down-regulated the expression of HMG-CoA reductase (HMGCR) but upregulated the expression of LDL receptor (LDLR) in the livers of the HCD-fed rats. However, pineapple consumption had no effect on hepatic CYP7A1 in HCD-fed rats. This study indicates that pineapple consumption ameliorates hyperlipidaemia in hypercholesterolemic rats. This effect is primarily mediated through the inhibition of lipid synthesis via suppressing the expression of HMGCR, and the activation of lipoprotein clearance via up-regulating the expression of LDLR.

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