Dietary fatty acids and the regulation of plasma low density lipoprotein cholesterol concentrations
Dietary fatty acids and the regulation of plasma low density lipoprotein cholesterol concentrations
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DOI：
10.1093/jn/128.2.444s
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发表时间：
1998-02-01
影响因子：
4.2
通讯作者：
Dietschy, JM
中科院分区：
文献类型：
--
作者：
Dietschy, JM
过去25年的流行病学研究表明，膳食脂肪摄入水平与平均血清胆固醇值和冠心病（CHD）死亡率呈正相关。许多不同的研究者证明，除了总脂肪外，饮食中的脂肪酸组成也会影响人的血清总胆固醇（TC）。一般来说，饱和脂肪酸会升高血清胆固醇浓度，而不饱和脂肪酸会降低该值。受影响的脂蛋白组分主要是低密度脂蛋白（LDL-C）中携带的胆固醇水平。现在已经证明，LDL-C的稳态水平主要由肝脏中的代谢事件决定。随着进入体内的膳食胆固醇的量增加，肝细胞中的固醇库扩大，并且主要负责从血流中清除LDL-C的LDL受体（LDLR）下调。然而，当膳食胆固醇摄入量保持恒定时，长链饱和脂肪酸进一步抑制肝LDLR活性，而几种不饱和脂肪酸具有相应的作用。这些调节事件依赖于各种脂肪酸的可用性，以在胆固醇的调节和储存库之间转移细胞内胆固醇，并且这种作用由酰基辅酶A：胆固醇酰基转移酶（ACAT）介导。
Epidemiologic studies over the past 25 years have shown that the level of dietary fat intake is positively correlated with the average serum cholesterol value and mortality from coronary heart disease (CHD). A number of different investigators demonstrated that in addition to total fat, the fatty acid composition of diets influenced serum total cholesterol (TC) in humans, In general, saturated fatty acids were found to elevate the serum cholesterol concentration, and unsaturated fatty acids were found to decrease this value, The lipoprotein fraction mast affected was the level of cholesteral carried in low density lipoprotein (LDL-C). It has now been demonstrated that the steady-state level of LDL-C is predominantly dictated by metabolic events in the liver, As the amount of dietary cholesterol entering the body is increased, there is expansion of the sterol pool in the liver cell and down regulation of LDL receptors (LDLR) that are primarily responsible for clearing LDL-C from the blood stream, When dietary cholesterol intake is kept constant, however, long-chain saturated fatty acids further suppress hepatic LDLR activity, whereas several unsaturated fatty acids have the apposite effect, These regulatory events depend upon the availability of the Various fatty acids to shift intracellular cholesterol between a regulatory and storage pool of cholesterol, and this effect is mediated by the enzyme acyl-CoA:cholesterol acyltransferase (ACAT).