In:
Clinical Chemistry, Oxford University Press (OUP), Vol. 50, No. 3 ( 2004-03-01), p. 589-595
Abstract:
Background: In individuals heterozygous for ABCA1 transporter mutations, defective reverse cholesterol transport (RCT) causes low HDL-cholesterol and premature coronary heart disease (CHD). However, the extent to which impaired RCT underlies premature CHD in others with low HDL-cholesterol is not known. The primary acceptors of cell cholesterol are a minor subclass of lipid-poor pre-β-HDLs. These are generated during remodeling of α-HDLs, which account for almost all HDL-cholesterol. We studied the strength of the association of CHD with pre-β-HDL concentrations in Japanese men. Methods: Blood was collected from 42 men with clinical CHD and 44 healthy controls 40–70 years of age. Pre-β-HDL was assayed by crossed immunoelectrophoresis. Results: Cases had lower HDL-cholesterol (−23%), total apolipoprotein A-I (−26%), and pre-β-HDL (−55%; all P & lt;0.001) concentrations; lower pre-β-HDL:α-HDL ratios (−45%; P & lt;0.001); and higher plasma triglycerides (20%; P & lt;0.03) than the controls. On stepwise logistic regression, CHD was associated most strongly with pre-β-HDL concentrations. On ROC analysis, pre-β-HDL concentration discriminated between cases and controls better than any other lipoprotein measurement. When plasma was incubated for 16 h at 37 °C, mean (SD) pre-β-HDL increased by 47 (36)% in controls, but was unchanged in cases (group difference, P & lt;0.001). Conclusions: Our results suggest that inefficient RCT, secondary to a low pre-β-HDL concentration and production rate in plasma, contributes to premature CHD in Japanese men with low HDL-cholesterol.
Type of Medium:
Online Resource
ISSN:
0009-9147
,
1530-8561
DOI:
10.1373/clinchem.2003.029207
Language:
English
Publisher:
Oxford University Press (OUP)
Publication Date:
2004
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