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This version published online on December 20, 2005
Journal of Clinical Endocrinology & Metabolism, doi:10.1210/jc.2005-1895
A more recent version of this article appeared on March 1, 2006
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Submitted on August 23, 2005
Accepted on December 13, 2005

High-density Lipoprotein Transport in the Metabolic Syndrome: application of a new model for HDL particle kinetics

Juying Ji, Gerald F. Watts*, Anthony G. Johnson, Dick C. Chan, Esther MM Ooi, Kerry-Anne Rye, Adrian P. Serone, and P. Hugh R. Barrett

Lipoprotein Research Unit, School of Medicine and Pharmacology, University of Western Australia, The West Australian Institute for Medical Research, Perth, Western Australia; GlaxoSmithKline R & D, King of Prussia, PA, USA; Lipid Research Group, The Heart Research Institute, Sydney, Australia; Department of Medicine, University of Sydney, Sydney, Australia; Department of Medicine, University of Melbourne, Melbourne, Australia; James Lance GlaxoSmithKline Medicines Research Unit, Prince of Wales Hospital, Sydney, Australia

* To whom correspondence should be addressed. E-mail: gfwatts{at}cyllene.uwa.edu.au.

Context: Reduced high density lipoprotein (HDL) concentration in the metabolic syndrome (MetS) is associated with increased risk of diabetes and cardiovascular disease, and is related to defects in the kinetics of HDL apolipoprotein (apo) A-I and A-II.

Objective: The objective of the study was to investigate HDL apoA-I and apoA-II kinetics in non-diabetic men with MetS and lean controls by developing a model that describe the kinetics of LpA-I and LpA-I:A-II particles.

Design: Twenty three MetS men and 10 age-matched lean controls were investigated. ApoA-I and apoA-II tracer/tracee ratios were studied following intravenous d3-leucine administration using gas chromatography mass spectrometry.

Results: Compared with leans, MetS subjects had accelerated catabolism of LpA-I (P < 0.001), LpA-I:A-II (P = 0.005) and apoA-II (P = 0.005); production rate of LpA-I was also significantly elevated in MetS, so that the dominant changes in plasma concentrations were reduction in LpA-I:A-II (P < 0.001) and apoA-II (P < 0.05). Increased catabolism of LpA-I and LpA-I:A-II were directly related with increased waist circumference, hypertriglyceridaemia, low HDL cholesterol, small HDL particle size, hyperinsulinaemia and low phospholipid transfer protein (PLTP) activity; overproduction of LpA-I was significantly associated with increased waist-circumference, insulin resistance and low PLTP activity.

Conclusions: MetS men exhibit hypercatabolism of the two major HDL lipoprotein particles, LpA-I and LpA-I:A-II, but selective overproduction of LpA-I maintains a "normal" plasma concentration of LpA-I. These kinetic perturbations are probably related to central obesity, insulin resistance, hypertriglyceridaemia and low plasma PLTP activity.
Key words: metabolic syndrome • high density lipoprotein • kinetics




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