Caloric restriction in rhesus monkeys reduces low density lipoprotein interaction with arterial proteoglycans
Caloric restriction in rhesus monkeys reduces low density lipoprotein interaction with arterial proteoglycans
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DOI：
10.1093/gerona/53a.6.b443
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发表时间：
1998-11-01
影响因子：
5.1
通讯作者：
Cefalu, WT
中科院分区：
文献类型：
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作者：
Edwards, IJ;Rudel, LL;Cefalu, WT
热量限制（CR）已被证明可以延缓许多物种的衰老过程。我们研究了 CR 对血浆低密度脂蛋白 (LDL) 的影响，LDL 是与年龄相关的动脉粥样硬化过程的主要危险因素。研究强调 CR 对 LDL 组成及其与动脉蛋白聚糖 (PG) 相互作用的影响。恒河猴被喂食对照饮食 (n = 13) 或接受 CR (n = 12 喂食热量减少 30%) 超过 5 个档次。对照组和 CR 组的血浆 LDL 胆固醇浓度相似（82 +/- 8 vs 72 +/- 6 mg/dL，平均值 +/- SEM）。通过超速离心和 HPLC 分离 LDL。来自 CR 动物的 LDL 颗粒具有较低的分子量（2.9 +/- 0.1 与 3.2 +/- 0.1 g/mu mol，p < .05），并且甘油三酯（249 +/- 16 与 433 +/- 49 mol/颗粒，p < .005）和磷脂（686 +/- 20 与 837 +/- 33 mol/颗粒）耗尽， p < .001)。对来自 CR 动物的 LDL 进行了较低的 PG 结合测量（10.1 +/- 0.8 vs 15.6 +/- 1.1 μg LDL 胆固醇/μg PG，p < .005）。这与较低的甘油三酯（r = .76，p < .0005）和磷脂（r = .48，p < .01）有关。因此，可以延缓衰老的饮食干预可以抑制动脉粥样硬化形成的机制。
Caloric restriction (CR) has been shown to retard aging processes in many species. We investigated effects of CR on plasma low density lipoproteins (LDL), a major risk factor for the age-associated process of atherosclerosis. Studies emphasized effects of CR on LDL composition and their interaction with arterial proteoglycans (PG). Rhesus monkeys were fed a control diet (n = 13) or subjected to CR (n = 12 fed 30% less calories) for > 5 gears. Plasma LDL cholesterol concentrations were similar for control and CR groups (82 +/- 8 vs 72 +/- 6 mg/dL, mean +/- SEM). LDL was isolated by ultracentrifugation and HPLC. LDL particles from CR animals had a lower molecular weight (2.9 +/- 0.1 vs 3.2 +/- 0.1 g/mu mol, p < .05) and were depleted in triglyceride (249 +/- 16 vs 433 +/- 49 mol/particle, p < .005) and phospholipid (686 +/- 20 vs 837 +/- 33 mol/particle, p < .001). Lower PG binding was measured for LDL from CR animals (10.1 +/- 0.8 vs 15.6 +/- 1.1 mu g LDL cholesterol/mu g PG, p < .005). This was associated with the lower triglycerides (r = .76, p < .0005) and phospholipids (r = .48, p < .01). Thus, a dietary intervention which may retard aging inhibits a proposed mechanism of atherogenesis.