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Papers In Press, published online ahead of print April 16, 2003
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Experimental Hepatology, Academic Medical Center Amsterdam, Amsterdam 1105BK
Corresponding Author: a.k.groen{at}amc.uva.nl
Objective. Defects in the gene encoding for the ATP Binding Cassette A1 (ABCA1) transporter were shown to be one of the genetic causes for familial hypoalphalipoproteinemia (FHA). We investigated the role of ABCA1 mediated cholesterol efflux in Dutch subjects suffering from FHA. Methods and Results: Eighty-eight subjects (mean HDL-c levels 0.63 ± 0.21 mmol/L) were enrolled. Fibroblasts were cultured and loaded with 3H-cholesterol. ABCA1 and non-ABCA1 mediated efflux was studied by using apoA-I, HDL and methyl-ß-cyclodextrin as acceptors. Efflux to apoA-I was decreased in four patients (4/88, 4.5 %) and in all cases a mutation in the ABCA1 gene was found. In the remaining 84 subjects no correlation between efflux to apoA-I and HDL-c was found. Efflux to both HDL and cyclodextrin, in contrast, did correlate with HDL-c plasma levels (r=0.34; p=0.01 and r=0.27; p=0.008 respectively). Conclusions: The prevalence of defects in ABCA1-dependent cholesterol efflux in Dutch FHA patients is low. The significant correlation between plasma HDL-c levels and methyl-ß-cyclodextrin mediated efflux in the FHA patients with normal ABCA1 function suggests that non-ABCA1 mediated efflux might also be important for plasma HDL-c levels in these individuals.
Revised on April 1, 2003
Accepted on April 1, 2003
The role of the ABCA1 transporter and cholesterol efflux in familial hypoalphalipoproteinemia
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