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Abstract
Objectives The purpose of this study was to explore the association between rs2292239 polymorphism in ERBB3 gene and type 1 diabetes (T1D). Methods A systematic search of studies on the association of rs2292239 polymorphism in ERBB3 gene with T1D susceptibility was conducted in PubMed, Web of science, Elsevier Science Direct, and Cochrane Library. Eventually, 9 published studies were included. The strength of association between rs2292239 polymorphism and T1D susceptibility was assessed by odds ratios (ORs) with its 95% confidence intervals (CIs). Results A total of 9 case-control studies, consisting of 5369 T1D patients and 6920 controls, were included in the meta-analysis. This meta-analysis showed significant association between ERBB3 rs2292239 polymorphism and T1D susceptibility in overall population (A vs. C, OR: 1.292, 95% CI= 1.224-1.364, PH=0.450, PH is P value for the heterogeneity test). Similar results were found in subgroup analysis by ethnicity. Conclusions ERBB3 rs2292239 polymorphism is associated with T1D susceptibility and rs2292239-A allele is a risk factor for T1D. However, more large-scale studies are warranted to replicate our findings.
Highlights
Type 1 diabetes (T1D), a kind of autoimmune disease, is characterized by the progressive loss of insulin-secreting pancreatic beta cells [1,2,3]
Nine studies involving 5369 T1D patients and 6920 controls were included in this meta-analysis
The ERBB gene might play a key role in immune regulation and cytokine-induced pancreatic beta-cell apoptosis, which related to T1D pathogenesis [19,20,21]
Summary
Type 1 diabetes (T1D), a kind of autoimmune disease, is characterized by the progressive loss of insulin-secreting pancreatic beta cells [1,2,3]. The etiology of T1D is very complex, which is affected by both genetic and environmental factors. It may occur at any age, compared with other age groups, the incidence of T1D in children is higher. The destruction of pancreatic beta-cells and the lack of insulin lead to hyperglycemia. T1D patients require exogenous insulin to survival. Those affected patients are insulin-dependent for life [6, 7].
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