Adiponectin and other adipocytokines as predictors of markers of triglyceride-rich lipoprotein metabolism

Background: Adipocytokines are bioactive peptides that may play an important role in the regulation of glucose and lipid metabolism. In this study, we investigated the association of plasma adipocytokine concentrations With markers of triglyceride-rich lipoprotein (TRL) metabolism in men. Methods: Fasting adiponectin, leptin, resistin, interleukin-6 IL-6), tumor necrosis factor-alpha (TNF-alpha), apolipoprotein (apo) B-48, apo C-III, and remnant-like particle (RLP)-cholesterol concentrations were measured by irnmunoassys and insulin resistance by homeostasis assessment (HOMA) score in 41 nondiabetic men with a body mass index of 22-35 kg/m(2). Visceral and subcutaneous adipose tissue masses (ATMs) were determined by magnetic resonance imaging and total ATM by bioelectrical impedance. Results: In univariate regression, plasma adiponectini and leptin concentrations were inversely and directly associated with Plasma apoB-48, apoC-III, RLP-cholesterol, triglycerides, VLDL-apoB, and VLDL-triglycerides (P <0.05). Resistin, IL-6, and TNF-alpha were not significantly associated with any of these variables, except for a direct correction between apoC-Ill and IL-6 (P <0.05). In multivariate regression including HOMA, age, nonesterified fatty acids, and adipose tissue compartment, adiponectin was an independent predictor of plasma apoB-48 (beta coefficient = -0.354; P = 0.048), apoC-III (beta coefficient = -0.406; P 0.012), RLP-cholesterol (beta coefficient = -0.377; P 0.016), and triglycerides (beta coefficient = -0.374; P = 0.013). By contrast, leptin was not an independent predictor of these TRL markers. Plasma apoB-48, apoC-III, RLP-cholesterol, and triglycerides were all significantly and positively associated with plasma insulin, HOMA, and visceral, subcutaneous, and total ATMs (P <0.05). Conclusions: These data suggest that the plasma adiponectin concentration may not only link abdominal fat, insulin resistance, and dyslipidemia, but may also exert an independent role in regulating TRL metabolism. (C) 2005 American Association for Clinical Chemistry.