Abstract
Prebeta-HDL particles act as the primary acceptors of cellular cholesterol in reverse cholesterol transport (RCT). An impairment of RCT may be the reason for the increased risk of coronary heart disease (CHD) in subjects with familial low HDL. We studied the levels of serum prebeta-HDL and the major regulating factors of HDL metabolism in 67 subjects with familial low HDL and in 64 normolipidemic subjects. We report that the subjects with familial low HDL had markedly reduced prebeta-HDL concentrations compared with the normolipidemic subjects (17.4 +/- 7.2 vs. 23.4 +/- 7.8 mg apolipoprotein A-I/dl; P < 0.001). A positive correlation was observed between prebeta-HDL concentration and serum triglyceride (TG) level (r = 0.334, P = 0.006). In addition, serum TG level was found to be the strongest predictor of prebeta-HDL concentration in subjects with familial low HDL. The activities of cholesteryl ester transfer protein and hepatic lipase were markedly increased in subjects with familial low HDL without a significant correlation to prebeta-HDL concentration. Our results support the hypothesis that impaired RCT is one mechanism behind the increased risk for CHD in subjects with familial low HDL.
Highlights
Pre-HDL particles act as the primary acceptors of cellular cholesterol in reverse cholesterol transport (RCT)
ApoA-I and lipoprotein A-I (LpA-I)/A-II were not included in the model because the amount of apolipoprotein A-I (apoA-I) is used in the calculation of the pre-HDL concentration
Thirty-one affected low-HDL family members had coronary heart disease (CHD) and 36 low-HDL family members were free of CHD
Summary
Pre-HDL particles act as the primary acceptors of cellular cholesterol in reverse cholesterol transport (RCT). An impairment of RCT may be the reason for the increased risk of coronary heart disease (CHD) in subjects with familial low HDL. The initial extracellular acceptors of cellular cholesterol are small lipid-poor apolipoprotein A-I (apoA-I) particles [3]. These particles, termed pre-HDL because of their electrophoretic mobility, represent either discoidal particles, consisting of two or three molecules of apoA-I complexed with phospholipids and unesterified cholesterol, or lipidfree apoA-I [4, 5]. There is evidence from in vitro studies that lipid-free/poor apoA-I is generated during the remodeling of HDL and that this form of apoA-I may play a fundamental role in the efflux of cholesterol from macrophage foam cells. Data on the existence of lipid-free/poor apoA-I in plasma in vivo is somewhat controversial (9, 9a)
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