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Journal of Diabetes Research
Volume 2016 (2016), Article ID 5412084, 12 pages
Review Article

Variations in the Obesity Gene “LEPR” Contribute to Risk of Type 2 Diabetes Mellitus: Evidence from a Meta-Analysis

1Eye Hospital, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China
2The Centre for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150001, China
3Department of Ophthalmology and Visual Sciences, The Chinese University of Hong Kong, Sha Tin 999077, Hong Kong
4Department of Endocrinology, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, China

Received 17 January 2016; Revised 21 March 2016; Accepted 24 March 2016

Academic Editor: Hassan Dashti

Copyright © 2016 Ming Ming Yang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Leptin is a hormone protein regulating food intake and energy expenditure. A number of studies have evaluated the genetic effect of leptin (LEP) and leptin receptor (LEPR) genes on T2DM. This study aimed to investigate the association between these gene polymorphisms and T2DM by a systematic review and meta-analysis. Published studies were identified through extensive search in PubMed and EMBASE. A total of 5143 T2DM cases and 5021 controls from 14 articles were included in this study. Five functional variants in LEPR were well evaluated. Meta-analysis showed that rs1137101 (p.R223Q) was significantly associated with T2DM in all genetic models: allele model (OR = 1.27, 95% confidence interval (CI) = 1.13–1.42), dominant model (OR = 1.19, 95% CI = 1.05–1.35), homozygote model (OR = 1.82, 95% CI = 1.38–2.39), and recessive model (OR = 1.75, 95% CI = 1.35–2.28), with minimal heterogeneity and no indication of publication bias. Similar associations with T2DM were also found for rs62589000 (p.P1019P) and 3′UTR ins/del, although the data was obtained from a small number of studies. For the other two polymorphisms rs1137100 (p.R109K) and rs8179183 (p.K656N), they were not significantly associated with T2DM. Our results provide robust evidences for the genetic association of rs1137101 (p.R223Q) in LEPR with T2DM susceptibility.