Ng Theodore W K, Watts Gerald F, Barrett P Hugh R, Rye Kerry-Anne, Chan Dick C
School of Medicine and Pharmacology, Metabolic Research Centre, University of Western Australia, New South Wales, Australia.
Diabetes Care. 2007 Nov;30(11):2945-50. doi: 10.2337/dc07-0768. Epub 2007 Aug 8.
The purpose of this study was to examine the effect of weight loss on LDL and HDL kinetics and plasma retinol-binding protein-4 (RBP-4) and adiponectin levels in men with the metabolic syndrome.
LDL apolipoprotein (apo)B-100 and HDL apoA-I kinetics were studied in 35 obese men with the metabolic syndrome at the start and end of a 16-week intervention trial of a hypocaloric, low-fat diet (n = 20) versus a weight maintenance diet (n = 15) using a stable isotope technique and multicompartmental modeling.
Consumption of the low-fat diet produced significant reductions (P < 0.01) in BMI, abdominal fat compartments, and homeostasis model assessment score compared with weight maintenance. These were associated with a significant increase in adiponectin and a fall in plasma RBP-4, triglycerides, LDL cholesterol, and LDL apoB-100 concentration (P < 0.05). Weight loss significantly increased the catabolism of LDL apoB-100 (+27%, P < 0.05) but did not affect production; it also decreased both the catabolic (-13%) and production (-13%) rates of HDL apoA-I (P < 0.05), thereby not altering plasma HDL apoA-I or HDL cholesterol concentrations. VLDL apoB-100 production fell significantly with weight loss (P < 0.05). The increase in LDL catabolism was inversely correlated with the fall in RBP-4 (r = -0.54, P < 0.05) and the decrease in HDL catabolism with the rise in adiponectin (r = -0.56, P < 0.01).
In obese men with metabolic syndrome, weight loss with a low-fat diet decreases the plasma LDL apoB-100 concentration by increasing the catabolism of LDL apoB-100; weight loss also delays the catabolism of HDL apoA-I with a concomitant reduction in the secretion of HDL apoA-I. These effects of weight loss could partly involve changes in RBP-4 and adiponectin levels.
本研究旨在探讨体重减轻对代谢综合征男性低密度脂蛋白(LDL)和高密度脂蛋白(HDL)代谢动力学以及血浆视黄醇结合蛋白-4(RBP-4)和脂联素水平的影响。
采用稳定同位素技术和多室模型,在35名患有代谢综合征的肥胖男性中,于低热量、低脂饮食(n = 20)与体重维持饮食(n = 15)的16周干预试验开始和结束时,研究LDL载脂蛋白(apo)B-100和HDL apoA-I的代谢动力学。
与体重维持组相比,低脂饮食组的体重指数(BMI)、腹部脂肪量和稳态模型评估得分显著降低(P < 0.01)。这些变化与脂联素显著增加以及血浆RBP-4、甘油三酯、LDL胆固醇和LDL apoB-100浓度下降相关(P < 0.05)。体重减轻显著增加了LDL apoB-100的分解代谢(+27%,P < 0.05),但不影响其生成;体重减轻还降低了HDL apoA-I的分解代谢率(-13%)和生成率(-13%)(P < 0.05),从而未改变血浆HDL apoA-I或HDL胆固醇浓度。体重减轻使极低密度脂蛋白(VLDL)apoB-100的生成显著下降(P < 0.05)。LDL分解代谢的增加与RBP-4的下降呈负相关(r = -0.54,P < 0.05),HDL分解代谢的降低与脂联素的升高呈负相关(r = -0.56,P < 0.01)。
在患有代谢综合征的肥胖男性中,低脂饮食导致的体重减轻通过增加LDL apoB-100的分解代谢降低血浆LDL apoB-100浓度;体重减轻还延缓了HDL apoA-I的分解代谢,并伴随HDL apoA-I分泌减少。体重减轻的这些作用可能部分涉及RBP-4和脂联素水平的变化。