Lipids in Health and Disease

Background: Apolipoprotein A-V (Apo A-V) gene has recently been identified as a new apolipoprotein involved in triglyceride metabolism. A single nucleotide polymorphism (SNP3) located in the gene promoter (-1131) was associated with triglyceride variation in healthy subjects. In type 2 diabetes the triglyceride level increased compared to healthy subjects. Hypertriglyceridemia is a risk factor for coronary artery disease. We aimed to examine the interaction between SNP3 and lipid profile and coronary artery disease (CAD) in Tunisian type 2 diabetic patients. Results: The genotype frequencies of T/T, T/C and C/C were 0.74, 0.23 and 0.03 respectively in non diabetic subjects, 0.71, 0.25 and 0.04 respectively in type 2 diabetic patients. Triglyceride level was higher in heterozygous genotype (-1131 T/C) of apo A-V (p = 0.024). Heterozygous genotype is more frequent in high triglyceride group (40.9%) than in low triglyceride group (18.8%) ; p = 0.011. Despite the relation between CAD and hypertriglyceridemia the SNP 3 was not associated with CAD. Conclusion: In type 2 diabetic patients SNP3 is associated with triglyceride level, however there was no association between SNP3 and coronary artery disease. Background Dyslipidemia in type 2 diabetes are most frequently characterized by elevation of total serum triglycerides, of very low density lipoprotein-triglyceride (VLDL-TG) and low level of high density lipoprotein-cholesterol (HDL-C) [1]. Hypertriglyceridemia is an independent risk factor for coronary artery disease (CAD) in type 2 diabetes [2]. Triglyceridemia is modulated by environmental and genetic factors. A new identified gene associated with triglyceride level was the gene encoding for apo A-V located at the chromosome 11 (11q23), in the vicinity of apoA-I/C-III/ A-IV cluster [3]. Studies on transgenic mice overexpressing human apo A-V showed a decreased level of triglyceride, whereas knock-out mice showed an increased level of Published: 06 January 2005 Lipids in Health and Disease 2005, 4:1 doi:10.1186/1476-511X-4-1 Received: 26 November 2004 Accepted: 06 January 2005 This article is available from: http://www.lipidworld.com/content/4/1/1 © 2005 Chaaba et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.