Xia · PloS one 2012 · systematic review and meta-analysis · n=172,963 participants (23 studies)

Association between the melatonin receptor 1B gene polymorphism on the risk of type 2 diabetes, impaired glucose regulation: a meta-analysis.

Cited 62 times in the scientific literature.

Level 3 - non-randomized controlled study

Systematic review and meta-analysis of observational genetic association studies

PubMed 23226241 · doi:10.1371/journal.pone.0050107 · record verified 2026-08-30

What was done

The authors conducted a systematic review and meta-analysis searching PubMed, EMBASE, ISI Web of Science, and CNKI to assess the relationship between two melatonin receptor 1B (MTNR1B) gene polymorphisms (rs10830963 and rs1387153) and the risk of type 2 diabetes (T2D) and impaired glucose regulation. Random-effects per-allele odds ratios (ORs) and 95% confidence intervals (CIs) were calculated along with tests for heterogeneity and publication bias.

What was found

A total of 23 studies comprising 172,963 subjects were analyzed. The rs10830963 polymorphism was significantly associated with T2D risk (per-allele OR = 1.05, 95% CI: 1.02–1.08, P < 0.0001) and with impaired glucose regulation susceptibility. The rs1387153 polymorphism showed no statistically significant overall association with T2D (per-allele OR = 1.04, 95% CI: 0.98–1.10, P = 0.20). Substantial heterogeneity was observed across studies; upon ethnic stratification, the rs10830963 association remained statistically significant in Caucasians but was not significant in East Asian or South Asian populations.

Why it matters

This study pools large-scale genetic data to confirm that common genetic variation in MTNR1B (rs10830963) contributes modestly to type 2 diabetes and impaired glucose regulation risk, highlighting population-specific genetic risk profiles.

Limits

The observed effect size was very small (OR 1.05). Significant heterogeneity was present in the overall analysis. The abstract does not detail specific study designs of the included papers (e.g., case-control vs. prospective cohort), diagnostic criteria applied across individual studies, or potential gene-environment interactions.

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