Seon-Min Jeon1, Yong Bok Park, Myung-Sook Choi. 1. Department of Nutrition and Food Science, Kyungpook National University, 1370 Sankyuk Dong Puk-ku, 702-701, Daegu 702-701, South Korea.
Abstract
BACKGROUND & AIMS: Hyperlipidemia is a major risk factor for cardiovascular diseases. This study was designed to confirm the hypocholesterolemic role of naringin. METHODS: Male rabbits were fed 0.5% high-cholesterol diet or high-cholesterol diet supplemented with either 0.05% naringin or 0.03% lovastatin for 8 weeks. RESULTS: The naringin and lovastatin supplements significantly lowered plasma total- and LDL-cholesterol and hepatic lipids levels, while significantly increasing HDL-C/total-C ratio compared to the control group. Hepatic 3-hydroxy-3-methylglutaryl CoA reductase and acyl-CoA: cholesterol acyltransferase activities were significantly higher and lower, respectively, in both supplemented groups than the control group. Total fecal sterol content was significantly increased in lovastatin and especially naringin group. In histopathological analyses, only control group exhibited hepatic lipid droplets, cardiac adipocyte infiltration and slight damage of endothelial lining in aortic wall, but two supplements retarded these atherogenic signs. CONCLUSION: It would appear that both naringin and lovastatin contributed to hypocholesterolemic action via down-regulated ACAT activity and higher excretion of fecal sterols in response to high-cholesterol feeding. Also, naringin supplement seemed to preserve tissue morphology from damages induced by high cholesterol diet.
BACKGROUND & AIMS:Hyperlipidemia is a major risk factor for cardiovascular diseases. This study was designed to confirm the hypocholesterolemic role of naringin. METHODS: Male rabbits were fed 0.5% high-cholesterol diet or high-cholesterol diet supplemented with either 0.05% naringin or 0.03% lovastatin for 8 weeks. RESULTS: The naringin and lovastatin supplements significantly lowered plasma total- and LDL-cholesterol and hepatic lipids levels, while significantly increasing HDL-C/total-C ratio compared to the control group. Hepatic 3-hydroxy-3-methylglutaryl CoA reductase and acyl-CoA: cholesterol acyltransferase activities were significantly higher and lower, respectively, in both supplemented groups than the control group. Total fecal sterol content was significantly increased in lovastatin and especially naringin group. In histopathological analyses, only control group exhibited hepatic lipid droplets, cardiac adipocyte infiltration and slight damage of endothelial lining in aortic wall, but two supplements retarded these atherogenic signs. CONCLUSION: It would appear that both naringin and lovastatin contributed to hypocholesterolemic action via down-regulated ACAT activity and higher excretion of fecal sterols in response to high-cholesterol feeding. Also, naringin supplement seemed to preserve tissue morphology from damages induced by high cholesterol diet.
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