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Abstract

Adiponectin has been schown to protect from insulin resistance, demonstrate anti-inflammatory and anti-atherosclerotic effects and be involved in the pathogenesis of metabolic syndrome (MS). We aimed to assess the association between serum adiponectin concentration, insulin resistance and various risk factors of MS and to investigate the relationship between the single nucleotide polymorphism (SNP) +45 T>G ( rs 2241766) in the adiponectin (ADIPOQ) gene and the risk of MS. 200 patients with MS and 250 healthy controls were enrolled in this study. The level of fasting serum insulin, glucose, and lipid levels were measured. Insulin resistance was estimated using homeostasis model of assessment for insulin resistance (HOMA-IR). Serum adiponectin levels were measured by enzyme-linked immunosorbent assay and the SNP +45 T>G in the ADIPOQ gene was performed by the polymerase chain reaction-restriction fragment length polymorphism method. MS patients had a significantly higher levels of HOMA-IR (p<0.001) and lower serum adiponectin concentrations (p<0.001) compared to controls. Multiple regression analysis showed that serum adiponectin levels was associated negatively with HOMA-IR (r=-0.307; p=0.001) and positively with high-density lipoprotein cholesterol (HDL-C) (r=0.369; p=0.000) in MS patients. In addition, there was no significant association between genotypes of rs 2241766 and the risk of MS. In conclusion, adiponectin is known to play key regulator of insulin sensitivity, endothelial function and lipid metabolism. Our findings confirm the associations of hypoadiponectinemia with MS and gave evidence that the SNP+45 T>G polymorphism in the gene of ADIPOQ is not associated with MS.

Association between +45T>G adiponectin polymorphism gene and type 2 diabetes mellitus and metabolic syndrome in a Venezuelan population

“…Regarding the alleles, a higher frequency of the T allele was observed over the G allele in both study groups, the T allele being more frequent in the population with MS-DM2, where the Hardy-Weinberg balance χ 2 = 5.99 is met, because the observed allele frequencies are as expected. Such findings relate to the MS population studied in Tunisia 28 but differ with the type 2 diabetes mellitus individuals studied in Brazil, India and Ireland 26, 27, 31 since the highest frequency of the T allele occurred in the healthy control group Table 4.…”

“…Moreover, Sahli et al . 28 reported statistically significant differences in BMI, fasting glucose, TC, TG, HDL-c, LDL-c, DBP, and SBP in a Tunisian population. However, a DM2 Chinese Han population 29 , showed no significant difference when comparing height and usCRP in diabetic and healthy control groups.…”

“…The same phenomenon was described in diabetics and non-diabetics in Northern India 34 ; however, no association between +45 T/G polymorphism and the development of DM2 was found in Koreans individuals with and without DM2 37 . The G allele of the +45 T>G polymorphism of the ADIPOQ gene has been associated with endocrine-metabolic pathology in Chinese individuals with and without MS in a similar population, whereas in Tunisia no association of polymorphism with MS was found 28, 38 .…”

“…The T/T genotype was found in greater frequency in the total population, although patients with MS-DM2 showed a greater frequency, as described by Sahli et al . 28 in a Tunisian MS population. T/G and G/G genotypes were found in both groups but showed lower frequencies.…”

“…mRNA G allele transcripts vary, proving higher than those of T allele of heterozygous individuals. This suggests that promoter gene polymorphisms or other adiponectin gene regulatory elements could be involved in the decrease or increase of the expression of the studied adipokine, being able to affect the mRNA allowing the stability of the splice sites in the same, affecting the amount of circulating proteins 28, 30 . It has also been observed that haplotypes that are in ligation unbalance with one or more functional variants can affect the levels of adiponectin in plasma, producing for example a change in the secondary structure of DNA, having a major influence on transcription, processing or translation; however, this is hypothetical, since the exact genetic mechanisms responsible for the expression of the specific allele have not been elucidated yet 32 .…”