Parks J S, Rudel L L
J Lipid Res. 1982 Mar;23(3):410-21.
Monkeys fed polyunsaturated fat had significantly lower plasma cholesterol (186 +/- 18 vs. 276 +/- 31 mg/dl) and high density lipoprotein (HDL) mass concentrations (466 +/- 28 vs. 518 +/- 34 mg/dl) than did animals fed saturated fat. Plasma apoA-I concentrations also were significantly lower and apoA-II levels were generally, though not significantly, lower in the group fed polyunsaturated fat. In vivo reinjection studies, using thoracic duct lymph chylomicra labeled with (131)I and HDL labeled with (125)I, were done in order to study the mechanism of plasma HDL-lowering by polyunsaturated dietary fat. The peak specific activity (SA) of HDL apoA-I derived from (131)I-labeled chylomicra occurred at 3 hr after injection (172 +/- 11% of 1 min S.A.) and then an exponential decay occurred indicative of a precursor-product relationship between chylomicron apoA-I and HDL apoA-I. In contrast, HDL apoA-II derived from (131)I-labeled chylomicra had no early S.A. increase and began to die away immediately after injection. Labeled apoA-I from chylomicron and HDL origin had similar plasma fractional catabolic rates (FCR = 0.34-0.38 vs. 0.32-0.38 d(-1), respectively); apoA-II from chylomicron or HDL origin also had similar FCR (0.46-0.51 vs. 0.42-0.51 d(-1), respectively), which were significantly shorter than those for HDL apoA-I. There was a consistent trend toward a higher FCR for HDL apoA-I or A-II of polyunsaturated fat-fed recipients. Chylomicron apoA-I/triglyceride and apoA-II/triglyceride mass ratios were lower in polyunsaturated fat-fed animals (A-I/TG = 1.56 x 10(-3); A-II/TG = 1.47 x 10(-3)) vs. saturated fat-fed animals (A-I/TG = 2.58 x 10(-3); A-II/TG = 2.77 x 10(-3)). It was concluded that: (1) dietary polyunsaturated fat significantly lowered plasma cholesterol, HDL, and apoA-I concentrations relative to saturated fat; (2) the HDL-lowering effect of the dietary polyunsaturated fat may be due to the combined effects of decreased apoprotein production by the intestine and increased HDL catabolism; and (3) in the blood, chylomicron apoA-I and A-II differ in their metabolic fates.-Parks, J. S., and L. L. Rudel. Different kinetic fates of apolipoproteins A-I and A-II from lymph chylomicra of nonhuman primates. Effect of saturated versus polyunsaturated dietary fat.
与喂食饱和脂肪的动物相比,喂食多不饱和脂肪的猴子血浆胆固醇(186±18 vs. 276±31 mg/dl)和高密度脂蛋白(HDL)质量浓度(466±28 vs. 518±34 mg/dl)显著降低。喂食多不饱和脂肪组的血浆载脂蛋白A-I浓度也显著降低,载脂蛋白A-II水平总体上虽不显著但也较低。为了研究多不饱和膳食脂肪降低血浆HDL的机制,进行了体内再注射研究,使用用(131)I标记的胸导管淋巴乳糜微粒和用(125)I标记的HDL。源自(131)I标记乳糜微粒的HDL载脂蛋白A-I的峰值比活性(SA)在注射后3小时出现(为1分钟SA的172±11%),然后呈指数衰减,表明乳糜微粒载脂蛋白A-I与HDL载脂蛋白A-I之间存在前体-产物关系。相比之下,源自(131)I标记乳糜微粒的HDL载脂蛋白A-II没有早期SA增加,注射后立即开始下降。来自乳糜微粒和HDL来源的标记载脂蛋白A-I具有相似的血浆分数分解代谢率(FCR分别为0.34 - 0.38 vs. 0.32 - 0.38 d(-1));来自乳糜微粒或HDL来源的载脂蛋白A-II也具有相似的FCR(分别为0.46 - 0.51 vs. 0.42 - 0.51 d(-1)),这明显短于HDL载脂蛋白A-I的FCR。喂食多不饱和脂肪的受体的HDL载脂蛋白A-I或A-II的FCR有一致的升高趋势。与喂食饱和脂肪的动物相比,喂食多不饱和脂肪的动物乳糜微粒载脂蛋白A-I/甘油三酯和载脂蛋白A-II/甘油三酯质量比更低(A-I/TG = 1.56×10(-3);A-II/TG = 1.47×10(-3))vs. (A-I/TG = 2.58×10(-3);A-II/TG = 2.77×10(-3))。得出以下结论:(1)相对于饱和脂肪,膳食多不饱和脂肪显著降低血浆胆固醇、HDL和载脂蛋白A-I浓度;(2)膳食多不饱和脂肪降低HDL的作用可能是由于肠道载脂蛋白产生减少和HDL分解代谢增加的综合作用;(3)在血液中,乳糜微粒载脂蛋白A-I和A-II的代谢命运不同。-帕克斯,J. S.,和L. L. 鲁德尔。非人类灵长类动物淋巴乳糜微粒中载脂蛋白A-I和A-II的不同动力学命运。饱和与多不饱和膳食脂肪的影响