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

Associations with changes in plasma retinol-binding protein-4 and adiponectin levels

  1. Theodore W.K. Ng, BSC1,
  2. Gerald F. Watts, MD, DSC1,
  3. P. Hugh R. Barrett, PHD1,
  4. Kerry-Anne Rye, PHD23 and
  5. Dick C. Chan, PHD1
  1. 1School of Medicine and Pharmacology, Metabolic Research Centre, University of Western Australia, New South Wales, Australia
  2. 2Lipid Research Group, The Heart Research Institute, University of Sydney, Sydney, New South Wales, Australia
  3. 3Department of Medicine, University of Sydney, Sydney, New South Wales, Australia
  1. Address correspondence and reprint requests to Prof. Gerald F. Watts, School of Medicine and Pharmacology, Metabolic Research Centre, Royal Perth Hospital, GPO Box X2213, Perth WA6847, Australia. E-mail: gerald.watts{at}uwa.edu.au


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.


  • Published ahead of print at http://care.diabetesjournals.org on 8 August 2007. DOI: 10.2337/dc07-0768.

    A table elsewhere in this issue shows conventional and Système International (SI) units and conversion factors for many substances.

    The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C Section 1734 solely to indicate this fact.

    • Accepted July 25, 2007.
    • Received April 20, 2007.
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  1. Diabetes Care vol. 30 no. 11 2945-2950
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