Increasing interest has been directed toward the role of the adiponectin gene polymorphism in the human genome and its implication in the pathogenesis of coronary artery disease. The present study was investigating the association between the single nucleotide polymorphism +276 G/T of the adiponectin gene with serum adiponectin level in patients with coronary artery disease (CAD). In this study 100 healthy controls and 100 Egyptian patients with coronary artery disease of both genders presented to the Cardiology Department of Suez Canal University Hospital were investigated. All subjects were genotyped for +276 G/T polymorphism of adiponectin gene.
Lipid profile, fasting blood glucose were measured. Adiponectin and high sensitivity C-reactive protein levels were determined by ELISA technique. Polymerase chain reaction based on restriction fragment length polymorphism (PCR-RFLP) was used to determine the genotypes of the studied population. The lowest serum adiponectin value was observed in patients with CAD compared with control group. The T alíele of SNP +276 G/T in the adiponectin gene was found to be associated with CAD (odd ratio 2.23; 95% CI: 1.
44-3.45; P= 0.001). The significant association of the T alíele (GT+TT) of this SNP with lower Correspondence ßutHor (dinawaliadan@yafioo.
com) 155 . Çfiattas et aCC adiponectin level and higher hsCRP levels was confirmed in the study (p= 0.003 and 0.006 respectively). Our results concluded that, +276 G/T SNP in the adiponectin gene is associated with CAD.
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Furthermore, carriers of the at-risk T alíele had lower serum adiponectin level and’ higher serum hsCRP, causing in turn an increased risk to develop CAD. Key Words: Adiponectin gene; polymorphism; Coronary artery disease; PCR-RFLP INTRODUCTION The adipose tissue has traditionally been regarded as a silent organ that is passively stores excess energy (such as triacylglycerol). However, recent evidence suggests that adipose tissue, especially visceral fat tissue, is considered as an endocrine organ, directly involved in the pathophysiology of the metabolic syndrome and cardiovascular diseases. In fact, visceral fat accumulation has recently been recognized as a key player in the occurrence of multiple risk factors for coronary artery disease (CAD) and in vascular changes (Matsuzawa, 2005).
Adiponectin is an adipocytokine, secreted fi^om white adipose tissue. It is a 30 kDa collagen like protein, clinically noted to be antiatherogenic and antidiabetic at elevated levels (Shibata et al., 2009). The average plasma concentration of this hormone ranges’ between 5 and 10 ^g/ml, levels vary according to sex, body fat distribution, and metabolic status (Salmenniemi et al., 2006). Low adiponectin has been linked to t’he presence of CAD (Kumada et al., 2003) and has been shown to be a risk factor for cardiovascular events (Giannessi et al., 2007).
Hypoadiponectinemia is strongly linked to central adiposity, dyslipidemia, insulin resistance and high blood pressure (Weyer et al., 2001; Trujillo and Scherer, 2005) Adiponectm also has anti-inflammatory properties affecting the nuclear factor (NF)-a pathway and inhibiting monocyte adhesion to aortic endothehal cells (Ouchi and Walsh, 2007). Many gene association studies showed that single nucleotide polymorphisms (SNPs) of adiponectin gene affect the adiponectin production in adipose tissue and modulate circulating adiponectin, but results are controversial and inconsistent (Yang and Chuang 2006) SNP +276 G/T (rs 1501299) has been associated with low’ serum adiponectin level, insulin resistance, and diabetes (Hara et al., 2002). 156 One can postulate that this SNP may also play a role in regulating the risk of CAD. Therefore the aim of this study was to investigate the association between SNP +276G/T of the adiponectin gene with serum adiponectin level in patients with CAD in a case-control study among Egyptians in Suez Canal area.The adipose tissue has traditionally been regarded as a silent organ that is passively stores excess energy (such as triacylglycerol). However, recent evidence suggests that adipose tissue, especially visceral fat tissue, is considered as an endocrine organ, directly involved in the pathophysiology of the metabolic syndrome and cardiovascular diseases.
In fact, visceral fat accumulation has recently been recognized as a key player in the occurrence of multiple risk factors for coronary artery disease (CAD) and in vascular changes (Matsuzawa, 2005). Adiponectin is an adipocytokine, secreted fi^om white adipose tissue. It is a 30 kDa collagen like protein, clinically noted to be antiatherogenic and antidiabetic at elevated levels (Shibata et al., 2009). The average plasma concentration of this hormone ranges’ between 5 and 10 ^g/ml, levels vary according to sex, body fat distribution, and metabolic status (Salmenniemi et al.
, 2006). Low adiponectin has been linked to t’he presence of CAD (Kumada et al., 2003) and has been shown to be a risk factor for cardiovascular events (Giannessi et al., 2007). Hypoadiponectinemia is strongly linked to central adiposity, dyslipidemia, insulin resistance and high blood pressure (Weyer et al., 2001; Trujillo and Scherer, 2005) Adiponectm also has anti-inflammatory properties affecting the nuclear factor (NF)-a pathway and inhibiting monocyte adhesion to aortic endothehal cells (Ouchi and Walsh, 2007).
Many gene association studies showed that single nucleotide polymorphisms (SNPs) of adiponectin gene affect the adiponectin production in adipose tissue and modulate circulating adiponectin, but results are controversial and inconsistent (Yang and Chuang 2006) SNP +276 G/T (rs 1501299) has been associated with low’ serum adiponectin level, insulin resistance, and diabetes (Hara et al., 2002). 156 One can postulate that this SNP may also play a role in regulating the risk of CAD. Therefore the aim of this study was to investigate the association between SNP +276G/T of the adiponectin gene with serum adiponectin level in patients with CAD in a case-control study among Egyptians in Suez Canal areaDISCUSSION Coronary artery diseases (CAD) constitute a major health problem in many parts of the world and are an important cause of morbidity and mortality. It is predicted that by the year 2020, CAD will be the main cause of disability worldwide (WHO, 2008). Previous studies regarding the genetic association of adiponectin gene +276 G/T SNP and the concomitant presence of CAD have been few, with nearly no report from Egyptian population.
Moreover, the overall reported associations of 276 G/T polymorphism and cardiometabolic disease were diverse. The present study provides evidence of association between the +276 G/T SNP of the adiponectin gene and CAD in this sample of Egyptian population. More precisely, a significant relation of minor T alíele with the presence of CAD was approved (0R= 2.2, CI= 1.44-3.
45, P= 0.001). In accordance with the findings of the present study, Filippi et al (2005) first reported that T alíele of 276 G/T is associated with higher risk of CAD than G alíele carriers. Another study on Saudi population confirmed the same findings (Mackawy et al.
, 2011). However, other studies have reported opposite results (Iacobellis et al., 2006; Leu et al., 2011) providing direct evidence that the major G alíele of 276 G/T of 162 A
