TY - JOUR
T1 - Adipocytokines and VLDL Metabolism : Independent Regulatory Effects of Adiponectin, Insulin Resistance, and Fat Compartments on VLDL Apolipoprotein B-100 Kinetics?
AU - Ng, Theodore Wai
AU - Watts, Gerald
AU - Farvid, M.S.
AU - Chan, Dick
AU - Barrett, Hugh
PY - 2005
Y1 - 2005
N2 - 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-[C-13]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.
AB - 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-[C-13]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.
UR - https://www.scopus.com/pages/publications/14644410377
U2 - 10.2337/diabetes.54.3.795
DO - 10.2337/diabetes.54.3.795
M3 - Article
SN - 0012-1797
VL - 54
SP - 795
EP - 802
JO - Diabetes
JF - Diabetes
IS - 3
ER -