Effects of dietary cholesterol and triglycerides on lipid concentrations in liver, plasma, and bile.
Effects of dietary cholesterol and triglycerides on lipid concentrations in liver, plasma, and bile.
复制标题
膳食胆固醇和甘油三酯对肝脏、血浆和胆汁中脂质浓度的影响。
DOI：
10.1007/s11745-997-0021-4
复制
发表时间：
1997
期刊：
影响因子：
1.9
通讯作者：
Hopkins,SR
中科院分区：
文献类型：
--
作者：
Booker,ML;LaMorte,WW;Beer,ER;Hopkins,SR
饮食中的胆固醇(CHL)和甘油三酯(TG)可以影响血浆、肝脏和胆汁中的脂质成分，但在CHL胆结石形成的早期阶段对这三个部分中的脂质的影响还没有平行研究。我们给草原犬饲喂含有四种TES油(红花、椰子、橄榄或薄荷)中的一种的饲料，热量的5%或40%，在0或0.34%的CHL存在下，持续3wk。在不添加CHL的情况下，增加日粮甘油三酯使胆汁CHL和肝脏胆固醇酯(CE)浓度增加50-200%，而肝脏游离CHL(FC)和血浆FC和CE浓度相对保持不变。将膳食CHL增加到0.34%会导致所有四种脂肪的肝脏FC增加约50%，无论它们是以5%的卡路里还是40%的卡路里供应。补充CHL导致胆汁CHL(200-400%)、肝脏CE(50-200%)、血浆Fc(高达100%)和血浆CE(高达150%)的显著增加，而同时补充膳食脂肪和CHL(胆汁CHL：300-700%；肝脏CE：100-250%；血浆FC：高达165%；血浆CE：100-350%)加剧了这些增加。这些结果表明，胆汁CHL分泌增加和肝脏CE合成增加可能是维持肝脏FC池的主要机制。此外，膳食CHL和高脂肪摄入量是胆汁CHL浓度增加的独立危险因素，而摄入富含脂肪和CHL的饮食往往会加剧对血浆和胆汁中脂质浓度的不利影响。
Dietary cholesterol (CHL) and triglycerides (TG) can influence plasma, hepatic, and biliary lipid composition, but effects on lipids in these three compartments during the early stages of CHL gallstone formation have not been studied in parallel. We fed prairie dogs diets containing one of four tes oils (safflower, coconut, olive, or menhaden) at either 5 or 40% of calories, in the presence of 0 or 0.34% CHL, for 3 wk. In the absence of dietary CHL, increases in dietary TG produced 50–200% increases in the concentrations of biliary CHL and hepatic cholesteryl ester (CE), while the concentrations of hepatic free CHL (FC) as well as plasma FC and CE remained relatively unchanged. Increasing dietary CHL to 0.34% resulted in increases in hepatic FC of approximately 50% for all four fats regardless of whether they were supplied at 5 or 40% of calories. CHL supplementation caused more pronounced increases in biliary CHL (200–400%), hepatic CE (50–200%), plasma FC (up to 100%), and plasma CE (up to 150%), and these increases were exacerbated by concurrent supplementation of dietary fat and CHL (biliary CHL: 300–700%; hepatic CE: 100–250%; plasma FC: up to 165%; plasma CE: 100–350%). These results indicate that enhanced secretion of biliary CHL and, to a lesser extent, increased synthesis of hepatic CE, may be primary mechanisms for maintaining the hepatic FC pool. Furthermore, dietary CHL and high levels of fat intake are independent risk factors for increasing biliary CHL concentrations, and adverse effects on lipid concentrations in plasma and bile tend to be exacerbated by ingestion of diets rich in both fat and CHL.