Abstract
Aims. Genetic association studies have reported the E23K variant of KCNJ11 gene to be associated with Type 2 diabetes. In Arab populations, only four studies have investigated the role of this variant. We aimed to replicate and validate the association between the E23K variant and Type 2 diabetes in Tunisian and Arab populations. Methods. We have performed a case-control association study including 250 Tunisian patients with Type 2 diabetes and 267 controls. Allelic association has also been evaluated by 2 meta-analyses including all population-based studies among Tunisians and Arabs (2 and 5 populations, resp.). Results. A significant association between the E23K variant and Type 2 diabetes was found (OR = 1.6, 95% CI = 1.14–2.27, and P = 0.007). Furthermore, our meta-analysis has confirmed the significant role of the E23K variant in susceptibility of Type 2 diabetes in Tunisian and Arab populations (OR = 1.29, 95% CI = 1.15–1.46, and P < 10−3 and OR = 1.33, 95% CI = 1.13–1.56, and P = 0.001, resp.). Conclusion. Both case-control and meta-analyses results revealed the significant association between the E23K variant of KCNJ11 and Type 2 diabetes among Tunisians and Arabs.
Highlights
Type 2 diabetes is a polygenic disorder characterized by defects in insulin secretion and peripheral insulin resistance [1]
Our meta-analysis has confirmed the significant role of the E23K variant in susceptibility of Type 2 diabetes in Tunisian and Arab populations (OR = 1.29, 95% confidence interval (95% CI) = 1.15–1.46, and P < 10−3 and Odd ratios (ORs) = 1.33, 95% CI = 1.13–1.56, and P = 0.001, resp.)
We have evaluated the association of the E23K variant in 250 Type 2 diabetes mellitus (T2DM) patients and 250 controls from Tunisian population
Summary
Type 2 diabetes is a polygenic disorder characterized by defects in insulin secretion and peripheral insulin resistance [1]. In the Tunisian population, the prevalence of Type 2 diabetes mellitus (T2DM) reaches 9% among adults [2] against 2.3% in 1977 [3]. These values showed an intermediate level compared to several human populations but they are still higher compared to European populations. It is well established that the potassium inwardly rectifying channel, subfamily J, member 11 (KCNJ11) gene located at chromosome 11p15.1 is involved in insulin secretion in humans and that mutations in this KCNJ11 gene can cause
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