Key result
Mutated genotypes at the adiponectin +276G/T locus were associated with a reduced risk of significant coronary stenosis (OR 0.472; 95% CI 0.195-0.842; P=0.046).
Why the study?
Do single-nucleotide polymorphisms at the adiponectin locus (+45T/G and +276G/T) affect the risk of significant coronary stenosis in Tunisian patients?
Observational (n=316)
Do single-nucleotide polymorphisms at the adiponectin locus (+45T/G and +276G/T) affect the risk of significant coronary stenosis in Tunisian patients?
Odds Ratio: 0.472 (95% CI 0.195–0.842)
p-value: p=0.046
In a Tunisian population, the +276G/T polymorphism at the adiponectin locus appears protective against significant coronary stenosis, whereas the +45T/G polymorphism increases risk specifically in obese individuals.
Should not yet inform clinical genotyping; extends adiponectin–stenosis associations to Tunisians but leaves causality and generalizability open.
OBJECTIVE: Adiponectin is an adipocyte-derived hormone and an essential modulator of insulin sensitivity. Several studies suggest an important role of adiponectin in the process leading to atherosclerosis, thus indicating the adiponectin gene as a potential candidate for coronary artery disease. Two single-nucleotide polymorphisms (SNPs) at the adiponectin locus (+45T/G and +276G/T) have been associated with low circulating adiponectin levels, insulin resistance and type 2 diabetes. The objective was to examine the association of two SNPs (45T/G and 276G/T) with coronary artery disease in a Tunisian population. METHODS: We have recruited 316 Tunisian patients, documented by coronary angiography. Significant coronary stenosis (SCS) was defined as a luminal narrowing of at least 50% in at least one major coronary artery. Genotyping was performed by polymerase chain reaction restriction fragment length polymorphism. Lipids and apolipoproteins were measured. RESULTS: After adjustments for confounder parameters, odds ratio (OR) of SCS associated with 276G/T mutated genotypes was 0.472 [95% confidence interval (CI) 0.195-0.842, P=0.046]. The mutated genotypes at the +45T/G polymorphism were significantly associated with increased SCS only in obese patients (OR 3.31, 95% CI 0.996-11.05, P=0.049 versus OR 1.71, 95% CI 0.467-6.269, P=0.418 in non-obese individuals). A potential protective effect was also observed for the haplogenotype TT/TT (OR 0.548, 0.306-0.982, P=0.043) in all the studied population. CONCLUSION: Mutated genotypes at +45T/G (GG + TG) were associated with an increase in SCS only in the obese group. Mutated genotypes at +276G/T (TT + GT) seem to reduce the risk of SCS in the studied population. When the two SNPs were combined, the TT/TT haplogenotype (normal genotype at 45T/G and mutated genotype at 276G/T) was associated with a protective effect.
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Boumaiza et al. (2011) conducted an observational in Coronary artery disease (n=316). Adiponectin locus SNPs (+45T/G and +276G/T) vs. Normal genotypes was evaluated on Significant coronary stenosis (SCS) (OR 0.472, 95% CI 0.195-0.842, p=0.046). Mutated genotypes at the adiponectin +276G/T locus were associated with a reduced risk of significant coronary stenosis (OR 0.472; 95% CI 0.195-0.842; P=0.046).
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