Abstract
The aim of this study was to ascertain the polymorphic markers profile of ADIPOQ,KCNJ11 and TCF7L2 genes in Kyrgyz population and to analyze the association of polymorphic markers and combinations of ADIPOQ gene's G276T locus, KCNJ11 gene's Glu23Lys locus and TCF7L2 gene's VS3C>T locus with type two diabetes (T2D) in Kyrgyz population. In this case‐control study, 114 T2D patients 109 non‐diabetic participants were genotyped using polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP). Two individual polymorphisms (ADIPOQ rs1501299, KCNJ11 rs5219) were found to be associated with T2D. We found two (Lys23Lys/CC and Glu23Lys/CT) of the overall nine combinations, which were more prevalent in T2D group compared to controls (χ2 = 4.21, P = 0.04). Lys23Lys/CC combination was associated with a 2.65‐fold increased likelihood of T2D (OR = 2.65, 95% CI 1.12‐6.28), whereas the Glu23Lys/CT combination also increased such likelihood (OR = 3.88, 95% CI 1.27‐11.91). This study demonstrated some association of 276T allele and ADIPOQ gene G276T heterozygous genotype as well as KCNJ11 gene 23Lys allele with T2D in ethnic Kyrgyz, but study results should be interpreted with caution because of the limited statistical power.
Highlights
Diabetes mellitus type 2 (T2D) is one of the major threats to human health because of its high prevalence, persistently growing prevalence and the severity of its late vascular complications if unrecognized and untreated.[1]
We found statistically significant differences in the distribution of genotypes and alleles of G276T polymorphic marker of ADIPOQ gene between cases and controls
G276T heterozygous genotype was associated with almost twofold higher risk of T2D (OR = 1.8, 95% confidence interval (CI) 1.05‐3.05), whereas 276T allele yielded the odds ratio (OR) 1.68
Summary
Diabetes mellitus type 2 (T2D) is one of the major threats to human health because of its high prevalence, persistently growing prevalence and the severity of its late vascular complications if unrecognized and untreated.[1]. Genetic predisposition to T2D was studied widely during the last decades.[2,3,4] At present, around 50 candidate genes are considered to increase the likelihood of T2D, of which adiponectin gene (ADIPOQ), potassium channel, inwardly rectifying subfamily J, member 11 (KCNJ11) and transcription factor 7‐like 2 (TCF7L2 [IVS3C>T]) may be associated with insulin resistance and β‐cells dysfunction.[5,6,7,8,9,10,11,12,13] Carriage of various SNP combinations may explain clinical heterogeneity of this disease. The analysis of cumulative SNP contribution in T2D is important
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