Research Center in Biological Sciences (NUPEB), Federal University of Ouro Preto, Ouro Preto, Minas Gerais, Brazil,
J Physiol Biochem. 2013 Dec;69(4):811-20. doi: 10.1007/s13105-013-0257-4. Epub 2013 May 5.
The present study investigated the underlying mechanism associated with the hypocholesterolemic activity of beta-carotene by examining its effects on the serum lipid profile, fecal cholesterol excretion, and gene expression of the major receptors, enzymes, and transporters involved in cholesterol metabolism. Female Fischer rats were divided into three groups and were fed either a control or a hypercholesterolemic diet supplemented or not supplemented with 0.2 % beta-carotene. After 6 weeks of feeding, blood, livers, and feces were collected for analysis, and quantitative real-time polymerase chain reaction (qRT-PCR) was performed. Dietary supplementation with 0.2 % beta-carotene decreased serum total cholesterol, non-HDL cholesterol, the atherogenic index, and hepatic total lipid and cholesterol contents. These changes were accompanied by an increase in the total lipid and cholesterol contents excreted in the feces. The qRT-PCR analyses demonstrated that the hypercholesterolemic diet promoted a decrease in the gene expression of sterol regulatory element-binding protein 2, 3-hydroxy-3-methylglutaryl CoA reductase, and low-density lipoprotein receptor and an increase in the gene expression of peroxisome proliferator-activated receptor α and cholesterol-7a-hydroxylase. The expression of these genes and gene expression of ATP-binding cassette subfamily G transporters 5and 8 were unaffected by beta-carotene supplementation. In conclusion, the decrease in serum cholesterol and the elevation of fecal cholesterol obtained following beta-carotene administration indicate that this substance may decrease cholesterol absorption in the intestine and increase cholesterol excretion into the feces without a direct effect on the expression of cholesterol metabolism genes.
本研究通过考察β-胡萝卜素对血清脂质谱、粪便胆固醇排泄以及胆固醇代谢主要受体、酶和转运体的基因表达的影响，研究了其降低胆固醇活性的潜在机制。将雌性 Fischer 大鼠分为三组，分别用对照饲料或高胆固醇饲料喂养，高胆固醇饲料添加或不添加 0.2%β-胡萝卜素。喂养 6 周后，采集血液、肝脏和粪便进行分析，并进行实时定量聚合酶链反应（qRT-PCR）。饮食补充 0.2%β-胡萝卜素可降低血清总胆固醇、非高密度脂蛋白胆固醇、动脉粥样硬化指数和肝总脂质及胆固醇含量。这些变化伴随着粪便中总脂质和胆固醇含量的增加。qRT-PCR 分析表明，高胆固醇饮食促进固醇调节元件结合蛋白 2、3-羟-3-甲基戊二酰辅酶 A 还原酶和低密度脂蛋白受体基因表达降低，过氧化物酶体增殖物激活受体 α 和胆固醇-7a-羟化酶基因表达增加。β-胡萝卜素补充对这些基因的表达和 ATP 结合盒亚家族 G 转运体 5 和 8 的基因表达没有影响。总之，β-胡萝卜素给药后血清胆固醇降低和粪便胆固醇升高表明，该物质可能通过减少肠道胆固醇吸收和增加胆固醇排泄到粪便中来降低胆固醇，而对胆固醇代谢基因的表达没有直接影响。
