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Abstract: P439 CHOLESTEROL EFFLUX CAPACITY AND ENDOTHELIAL FUNCTION IN TYPE 2 DIABETES MELLITUS
Poster - LIPOPROTEIN METABOLISM - Reverse Cholesterol Transport and HDL Metabolism Abstract: P439 Citation: Atherosclerosis Supplement 2009, Vol. 10, Issue 2
CHOLESTEROL EFFLUX CAPACITY AND ENDOTHELIAL FUNCTION IN TYPE 2 DIABETES MELLITUS K Tan, H Zhou, S Shiu, Y Wong Medicine, University of Hong Kong, Hong Kong Objective: Recent experimental data have suggested that impaired cholesterol efflux might cause endothelial dysfunction. Defective cholesterol efflux was associated with impaired endothelium-dependent vasodilation in ATP-binding cassette transporter A1 (ABCA1) or ABCG1 knock-out mice fed on a high cholesterol diet. We investigated whether the capacity of serum to induce cholesterol efflux was associated with changes in endothelial function in type 2 diabetic patients. Methods: 137 diabetic patients and 75 age-matched healthy controls were recruited. Serum cholesterol efflux capacity was determined by measuring the transfer of [3H]cholesterol from Fu5AH cells to the medium containing the tested serum. Endothelial function was assessed by measuring endothelium-dependent and -independent vasodilation of the brachial artery using high-resolution vascular ultrasound. Results: Serum cholesterol efflux capacity was lower in diabetic patients than controls (13.6 ± 2.5% vs. 14.6 ± 3.4% respectively, p<0.05), and both endothelium-dependent vasodilation (4.9 ± 2.2% vs. 8.8 ± 4.1% respectively, p<0.01) and endothelium-independent vasodilation (13.4 ± 4.3% vs. 16.3 ± 5.5% respectively, p<0.01) were impaired. Endothelium-dependent vasodilation correlated with serum cholesterol efflux capacity (r=0.26, p<0.01) but not with plasma lipids, apolipoproteins or C-reactive protein in the diabetic patients. On general linear model univariate analysis, brachial artery diameter, serum cholesterol efflux capacity and the presence of hypertension were significant independent determinants of endothelium-dependent vasodilation. Conclusion: In type 2 diabetic patients, impaired serum cholesterol efflux capacity was associated with endothelial dysfunction independent of other cardiovascular risk factors.
CHOLESTEROL EFFLUX CAPACITY AND ENDOTHELIAL FUNCTION IN TYPE 2 DIABETES MELLITUS K Tan, H Zhou, S Shiu, Y Wong Medicine, University of Hong Kong, Hong Kong Objective: Recent experimental data have suggested that impaired cholesterol efflux might cause endothelial dysfunction. Defective cholesterol efflux was associated with impaired endothelium-dependent vasodilation in ATP-binding cassette transporter A1 (ABCA1) or ABCG1 knock-out mice fed on a high cholesterol diet. We investigated whether the capacity of serum to induce cholesterol efflux was associated with changes in endothelial function in type 2 diabetic patients. Methods: 137 diabetic patients and 75 age-matched healthy controls were recruited. Serum cholesterol efflux capacity was determined by measuring the transfer of [3H]cholesterol from Fu5AH cells to the medium containing the tested serum. Endothelial function was assessed by measuring endothelium-dependent and -independent vasodilation of the brachial artery using high-resolution vascular ultrasound. Results: Serum cholesterol efflux capacity was lower in diabetic patients than controls (13.6 ± 2.5% vs. 14.6 ± 3.4% respectively, p<0.05), and both endothelium-dependent vasodilation (4.9 ± 2.2% vs. 8.8 ± 4.1% respectively, p<0.01) and endothelium-independent vasodilation (13.4 ± 4.3% vs. 16.3 ± 5.5% respectively, p<0.01) were impaired. Endothelium-dependent vasodilation correlated with serum cholesterol efflux capacity (r=0.26, p<0.01) but not with plasma lipids, apolipoproteins or C-reactive protein in the diabetic patients. On general linear model univariate analysis, brachial artery diameter, serum cholesterol efflux capacity and the presence of hypertension were significant independent determinants of endothelium-dependent vasodilation. Conclusion: In type 2 diabetic patients, impaired serum cholesterol efflux capacity was associated with endothelial dysfunction independent of other cardiovascular risk factors.