Effects of dietary cholesterol and fatty acids on plasma lipoproteins.

Effects of dietary cholesterol and fatty acids on plasma lipoproteins.
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膳食胆固醇和脂肪酸对血浆脂蛋白的影响。

DOI:
10.1172/jci110542
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发表时间:
1982
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Olson,RE
Olson,RE
中科院分区:
--
文献类型:
--
作者:
Schonfeld,G;Patsch,W;Rudel,LL;Nelson,C;Epstein,M;Olson,RE

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本文研究了20名青年男子膳食胆固醇和脂肪酸对低密度脂蛋白(LDL)和高密度脂蛋白(HDL)的影响。在2-3周的即兴评估后。基础日粮由15%蛋白质、4 - 5%碳水化合物、40%脂肪和300 mg/d胆固醇组成,持续4-5周(基础)。不同组受试者的膳食多不饱和脂肪酸与饱和脂肪酸的比率(P/S)分别为0.25、0.4、0.8或2.5。在基础日粮中分别添加750和1,500 mg/d的胆固醇,即3个和6个鸡蛋。基础饮食组的总胆固醇和低密度脂蛋白胆固醇均低于自由饮食组。节食。在P/S = 0.25-0.4的饮食中添加750 mg胆固醇使LDL胆固醇增加16 +/- 14 mg/dl至基础饮食值的115%(n = 11,P小于0.01); 1,500 mg使LDL胆固醇增加25 +/- 19 mg/dl至125%(n = 9,P小于0.01)。在P/S = 0.8的饮食中,750 mg导致LDL胆固醇无显著增加,但1,500 mg导致17 +/- 22 mg/dl增加至基础水平的115%(n = 6,P <0.02)。在P/S = 2.5的饮食中,750或1,500 mg均未产生显著变化。因此,胆固醇含量和P/S比的饮食是重要的,在确定LDL水平。脂质和载脂蛋白的组成,浮选率,分子量,并结合细胞受体的LDL几乎不变的胆固醇添加到高饱和脂肪的饮食。因此,这些饮食引起了LDL颗粒数量的增加,而这些颗粒的物理和生物特性几乎没有变化。在低P/S比的饮食中,HDL 2升高,而在高P/S比的饮食中不存在这种效应。低密度脂蛋白对饮食控制的反应与高胆固醇和饱和脂肪饮食与动脉粥样硬化形成相关的流行病学数据一致。然而,HDL 2的反应与其作为负性风险因素的假定作用相反。需要进一步的工作来澄清这个有趣的悖论。
The effects of dietary cholesterol and fatty acids on low density and high density lipoproteins (LDL and HDL) were studied in 20 young men. After 2-3 wk of evaluations on ad lib. diets, basal diets, which consisted of 15% protein, 45% carbohydrates, 40% fat, and 300 mg/day of cholesterol, were given for 4-5 wk (Basal). The ratio of dietary polyunsaturated to saturated fatty acids (P/S) for different groups of subjects were 0.25, 0.4, 0.8, or 2.5. 750 and 1,500 mg/d of cholesterol were added to the basal diets as 3 and 6 eggs, respectively. Total cholesterol and LDL cholesterol were lower in all subjects on the basal diets than on the ad lib. diets. Addition of 750 mg cholesterol to the diet with P/S = 0.25-0.4 raised LDL cholesterol by 16 +/- 14 mg/dl to 115% of basal diet values (n = 11, P less than 0.01); 1,500 mg increased LDL cholesterol by 25 +/- 19 mg/dl to 125% (n = 9, P less than 0.01). On the diet with P/S = 0.8, 750 mg produced insignificant increases in LDL cholesterol, but 1,500 mg produced increases of 17 +/- 22 mg/dl to 115% of basal (n = 6, P less than 0.02). On the P/S = 2.5 diet, neither 750 nor 1,500 mg produced significant changes. Thus, both the cholesterol contents and P/S ratios of diets were important in determining LDL levels. The lipid and apoprotein compositions, flotation rates, molecular weights, and binding by cellular receptors of LDL were virtually unchanged by the addition of cholesterol to the diets high in saturated fat. These diets, therefore, caused an increase in the number of LDL particles of virtually unchanged physical and biological properties. On the diet with low P/S ratio, HDL2 rose, whereas this effect was absent on diets with high P/S ratios. The response of LDL to dietary manipulations is consonant with epidemiologic data relating diets high in cholesterol and saturated fat to atherogenesis. The response of HDL2, however, is opposite to that of its putative role as a negative risk factor. Further work is needed to clarify this interesting paradox.
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