Effect of Weight Loss on LDL and HDL Kinetics in the Metabolic Syndrome  

Oleh:

Ng, Theodore W.K. ; Watts, Gerald F.M ; Barrett, P. Hugh R. ; Rye, Kerry-Anne ; Chan, Dick C.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 30 no. 11 (Nov. 2007), page 2945.
Topik: apo; apolipoprotein • ATM; adipose tissue mass • CETP; cholesteryl ester transfer protein • FCR; fractional catabolic rate • FFM; fat-free mass • HOMA; homeostasis model assessment • IDL; intermediate density lipoprotein • NEFA; nonesterified fatty acid • PLTP; phospholipid transfer protein • RBP-4; retinol-binding protein-4

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2007.04 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

OBJECTIVE—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. RESEARCH DESIGN AND METHODS—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. RESULTS—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). CONCLUSIONS—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.

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