Ng Theodore W K, Watts Gerald F, Farvid Maryam S, Chan Dick C, Barrett P Hugh R
School of Medicine and Pharmacology, Western Australian Institute for Medical Research, University of Western Australia, Perth, Western Australia 6847, Australia.
Diabetes. 2005 Mar;54(3):795-802. doi: 10.2337/diabetes.54.3.795.
We investigated the relationship of plasma adipocytokine concentrations with VLDL apolipoprotein B (apoB)-100 kinetics in men. Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22-35 kg/m(2). VLDL apoB kinetics were determined using an intravenous infusion of 1-[(13)C]leucine, gas chromatography-mass spectrometry, and compartmental modeling. Visceral and subcutaneous adipose tissue mass (ATM) were determined using magnetic resonance imaging, and total ATM was measured by bioelectrical impedance. In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride; HOMA score; and visceral, subcutaneous, and total ATMs. Conversely, adiponectin and leptin were directly and inversely correlated, respectively, with VLDL apoB catabolism and HDL cholesterol concentration (P < 0.05). Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables. In multivariate regression, adiponectin was the most significant predictor of plasma VLDL apoB concentration (P = 0.001) and, together with total or subcutaneous ATM, was an independent predictor of VLDL apoB catabolism (P < 0.001); HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P < 0.05). Leptin was not an independent predictor of VLDL apoB kinetics. In conclusion, plasma VLDL apoB kinetics may be differentially controlled by adiponectin and insulin resistance, with adiponectin regulating catabolism and insulin resistance regulating hepatic secretion in men. Total body fat may also independently determine the rate of VLDL catabolism, but leptin, resistin, IL-6, and TNF-alpha do not have a significant effect in regulating apoB kinetics.
我们研究了男性血浆脂肪细胞因子浓度与极低密度脂蛋白载脂蛋白B（apoB）-100动力学之间的关系。采用酶免疫分析法测定了41名体重指数（BMI）为22至35kg/m²的男性的血浆脂联素、瘦素、抵抗素、白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）浓度，并通过稳态模型评估（HOMA）评分评估胰岛素抵抗。使用静脉输注1-[(13)C]亮氨酸、气相色谱-质谱联用和房室模型测定极低密度脂蛋白apoB动力学。使用磁共振成像测定内脏和皮下脂肪组织量（ATM），并通过生物电阻抗测量总ATM。在单变量回归中，血浆脂联素和瘦素浓度分别与血浆甘油三酯、HOMA评分以及内脏、皮下和总ATM呈负相关和正相关。相反，脂联素和瘦素分别与极低密度脂蛋白apoB分解代谢和高密度脂蛋白胆固醇浓度呈正相关和负相关（P<0.05）。抵抗素、IL-6和TNF-α与这些变量均无显著相关性。在多变量回归中，脂联素是血浆极低密度脂蛋白apoB浓度的最显著预测因子（P = 0.001），并且与总或皮下ATM一起，是极低密度脂蛋白apoB分解代谢的独立预测因子（P<0.001）；HOMA评分是极低密度脂蛋白apoB肝脏分泌的最显著预测因子（P<0.05）。瘦素不是极低密度脂蛋白apoB动力学的独立预测因子。总之，男性血浆极低密度脂蛋白apoB动力学可能受脂联素和胰岛素抵抗的不同调控，脂联素调节分解代谢，胰岛素抵抗调节肝脏分泌。全身脂肪也可能独立决定极低密度脂蛋白分解代谢的速率，但瘦素、抵抗素、IL-6和TNF-α在调节apoB动力学方面没有显著作用。
