Association between two SNPs (+45T>G and +276G>T) of the adiponectin gene and coronary artery diseases.
- Author:
Chan Hee JUNG
1
;
Eun Jung RHEE
;
Se Yeon KIM
;
Hun Sub SHIN
;
Byung Jin KIM
;
Ki Chul SUNG
;
Bum Su KIM
;
Won Young LEE
;
Jin Ho KANG
;
Ki Won OH
;
Man Ho LEE
;
Sun Woo KIM
;
Jung Roe PARK
Author Information
1. Department of Internal Medicine, Sungkyunkwan University School of Medicine, Kangbuk Samsung Hospital, Seoul, Korea. hongsiri@hanmail.net
- Publication Type:Original Article
- Keywords:
Adiponectin;
Polymorphism;
Coronary artery disease
- MeSH:
Adiponectin*;
Alleles;
Blood Glucose;
Body Mass Index;
Chest Pain;
Cholesterol;
Compliance;
Coronary Artery Disease*;
Coronary Vessels*;
Fasting;
Female;
Gene Frequency;
Genetic Variation;
Genotype;
Glucose;
Humans;
Insulin Resistance;
Lipoproteins;
Male;
Obesity;
Polymerase Chain Reaction;
Polymorphism, Single Nucleotide*
- From:Korean Journal of Medicine
2006;70(4):393-401
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Adiponectin, an adipocyte-secreted protein, is known to have anti-atherogenic, anti-inflammatory and anti-diabetic properties. Adiponectin levels are decreased in obesity, type 2 diabetes, and coronary artery disease. Several studies have been performed aiming to investigate the association of genetic variations in the adiponectin with obesity, insulin resistance, and type 2 diabetes but few studies were performed in association with coronary artery disease. Therefore we examined the association between two single nucleotide polymorphisms (SNPs) (+45T>G and +276G>T) of the adiponectin gene and coronary artery diseases (CAD). METHODS: One hundred fifty six subjects were enrolled in which coronary angiograms were performed due to chest pain in Kangbuk Samsung Hospital from April to August, 2003 (97 males, 59 females, mean age 57.40+/-11.15 yrs). Body mass index, fasting blood glucose, lipid profiles were measured in every subject. Single nucleotide polymorphisms (SNPs) in the adiponectin gene were determined by Taqman polymerase chain reaction (PCR) method. The presence of CAD was defined as a >50% reduction of coronary artery diameter. RESULTS: Among 156 subjects, the allele frequencies were 0.683 for G allele and 0.317 for T allele in SNP +276G>T and 0.705 for T allele and 0.295 for G allele in SNP +45T>G. Both genotypes were in compliance with Hardy-Weinberg equlibrium. Mean serum fasting glucose level was significantly higher and mean high-density lipoprotein cholesterol (HDL-C) level was lower in CAD groups (p=0.015, p=0.004). No association with the presence of CAD was observed for adiponectin gene SNP276 and SNP45 (p=0.954, p=0.843). Also, no significant association was observed between the severity of CAD and either SNPs (p=0.571, p=0.955). CONCLUSIONS: Our study showed that SNP +276G>T and +45T>G in adiponectin gene were not associated with the presence of CAD. Further studies will be necessary to confirm the role of SNP 276G>T and 45T>G in the development of CAD.
