Association of SNP3 polymorphism in the apolipoprotein A-V gene with plasma triglyceride level in Tunisian type 2 diabetes

被引：18

作者：

Chaaba R. ^{[1
]}

Attia N. ^{[1
]}

Hammami S. ^{[2
]}

Smaoui M. ^{[1
]}

Mahjoub S. ^{[2
]}

Hammami M. ^{[1
]}

Masmoudi A.S. ^{[1
]}

机构：

[1] Biochemistry Laboratory, UR 08-39, Faculty of Medicine, Monastir

[2] Department of Internal Medicine, CHU, Monastir

来源：

Lipids in Health and Disease | / 4卷 / 1期

关键词：

Coronary Artery Disease; Triglyceride; Diabetic Patient; Triglyceride Level; Diabetic Subject;

D O I：

10.1186/1476-511X-4-1

中图分类号：

学科分类号：

摘要：

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. © 2005 Chaaba et al; licensee BioMed Central Ltd.

引用

共 15 条

[1]

Kreisberg R.A., Diabetic Dyslipidemia, Am J Cardiol, 82, (1998)

[2]

Lahdenpera S., Syvanne M., Kahri J., Taskinen M.R., Regulation of low density lipoprotein particle size distribution in NIDDM and coronary disease: Importance of serum triglycerides, Diabetologia, 39, pp. 453-461, (1996)

[3]

Pennacchio L.A., Olivier M., Hubacek J.A., Cohen J.C., Cox D.R., Fruchart J.C., Krauss R.M., Rubin E.M., An Apolipoprotein influencing Triglycerides in Humans and Mice revealed by Comparative Sequencing, Science, 294, pp. 169-173, (2001)

[4]

Vliet H.N., Van Der Schaap F.G., Levels J.H.M., Ottenhoff R., Looije N., Wesseling J.G., Groen A.K., Chamulleau R.A.F.M., Adenoviral overexpression of apolipoprotein A-V reduces serum levels of triglycerides and cholesterol in mice, Biochem Biophys Res Commun, 295, pp. 1156-1159, (2002)

[5]

Endo K., Yanagi H., Araki J., Hirano Ch., Yamakawa-Kobayashi K., Tomura Sh., Association found between the promoter region polymorphism in the apolipoprotein A-V gene and the serum triglyceride level in Japanese schoolchildren, Hum Genet, 111, pp. 570-572, (2002)

[6]

Esteve E., Faure E., Calvo F., Aguillo E., Blasco C., Roche M.J., Mozas P., Pocovi M., SNP3 polymorphism in apo A-V gene is associated with small dense LDL particles in type 2 diabetes, Diabetologia, 47, pp. 355-356, (2004)

[7]

Weinberg R.B., Cook V.R., Beckstead J.A., Martin D.O., Gallagher J.W., Shelness G.S., Ryan R.O., Structure and interfacial properties of human apolipoprotein A-V, J Biol Chem, 278, pp. 34438-34444, (2003)

[8]

Schaap F.G., Rensen P.C., Voshol P.J., Et al., Apo AV reduces plasma triglycerides by inhibiting very low density lipoprotein-triglyceride production and stimulating lipoprotein lipase-mediated VLDL-TG hydrolysis, J Biol Chem, 279, pp. 27941-27947, (2004)

[9]

Nabika N., Nasreen Sh., Kobayashi Sh., Masuda J., The genetic effect of the apoprotein AV gene on the serum triglyceride level in Japanese, Atherosclerosis, 165, pp. 201-204, (2002)

[10]

Talmud P.J., Hawe E., Martin S., Olivier M., Miller G.J., Rubin E.M., Pennacchio L.A., Humphries S.E., Relative contribution of variation within the APOC3/A4/A5 gene cluster in determining plasma triglycerides, Hum Mol Genet, 11, pp. 3039-3046, (2002)

← 1 2 →