Volume 5, Issue 3 (17 2006)
ijdld 2006, 5(3): 217-225 |
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Farvid M S, Ng T, D.C C, P.H.R B, G.F W. ADIPOCYTOKINES AND VLDL METABOLISM INDEPENDENT REGULATORY EFFECTS OF ADIPONECTIN, INSULIN RESISTANCE, AND FAT COMPARTMENTS ON VLDL APOLIPOPROTEIN B-100 KINETICS?. ijdld 2006; 5 (3) :217-225
URL: http://ijdld.tums.ac.ir/article-1-362-en.html
URL: http://ijdld.tums.ac.ir/article-1-362-en.html
Abstract: (52671 Views)
Background: Obesity is an escalating public health problem. It is a major risk factor for atherosclerosis, hypertension, and type 2 diabetes. Since circulating levels of the adipocytokins are associated with obesity and dyslipidemia, we investigated the relationship of plasma adipocytokine concentrations with VLDL apolipoprotein B (apoB)-100 kinetics in men.
Methods: Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22–35 kg/m2. VLDL apoB kinetics were determined using an intravenous infusion of 1-[13C]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.
Results: In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride and HOMA score. 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-α were not significantly associated with any of these variables. In multivariate regression, adiponectin was the most significant predictor of VLDL apoB catabolism (P= 0.001) and, together with visceral ATM, was an independent predictor of plasma VLDL apoB concentration (P = 0.015) HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P= 0.049). Leptin was not an independent predictor of VLDL apoB kinetics.
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. But leptin, resistin, IL-6, and TNF-α do not have a significant effect in regulating apoB kinetics.
Methods: Plasma adiponectin, leptin, resistin, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) concentrations were measured using enzyme immunoassays and insulin resistance by homeostasis model assessment (HOMA) score in 41 men with BMI of 22–35 kg/m2. VLDL apoB kinetics were determined using an intravenous infusion of 1-[13C]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.
Results: In univariate regression, plasma adiponectin and leptin concentrations were inversely and directly associated, respectively, with plasma triglyceride and HOMA score. 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-α were not significantly associated with any of these variables. In multivariate regression, adiponectin was the most significant predictor of VLDL apoB catabolism (P= 0.001) and, together with visceral ATM, was an independent predictor of plasma VLDL apoB concentration (P = 0.015) HOMA score was the most significant predictor of VLDL apoB hepatic secretion (P= 0.049). Leptin was not an independent predictor of VLDL apoB kinetics.
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. But leptin, resistin, IL-6, and TNF-α do not have a significant effect in regulating apoB kinetics.
Type of Study: Research |
Subject:
General
Received: 2006/01/2 | Accepted: 2006/05/3 | Published: 2013/10/3
Received: 2006/01/2 | Accepted: 2006/05/3 | Published: 2013/10/3
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