SynthesisPloS one2018
A meta-analysis of associations of LEPR Q223R and K109R polymorphisms with Type 2 diabetes risk.
Synthesis in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.
- Genetic predisposition of LEPR (rs1137101) gene polymorphism related to type 2 diabetes mellitus - a meta-analysis.Annals of medicine · 2023Pooled it
- Meta-analyses of IL1A polymorphisms and the risk of several autoimmune diseases published in databases.PloS one · 2018Pooled it
- Preliminary insight into the potential role of Leptin Receptor Polymorphisms in Type 2 Diabetes Risk: case-control study and bioinformatics analysis.Journal of diabetes and metabolic disorders · 2025Article
- Association of leptin receptor gene Gln223Arg polymorphism with insulin resistance and hyperglycemia in patients with metabolic syndrome.Archives of medical science : AMS · 2024Article
- Association of rs1137101 with hypertension and type 2 diabetes mellitus of Mongolian and Han Chinese.World journal of diabetes · 2022Article
- Polymorphisms in hormone-sensitive lipase and leptin receptor genes and their association with growth traits in Barki lambs.Veterinary world · 2021Article
- Review
- Variability in the leptin receptor gene and other risk factors for post-transplant diabetes mellitus in renal transplant recipients.Annals of medicine · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLeptin receptor (LEPR) plays a pivotal role in the control of body weight, energy metabolism, and insulin sensitivity. Various genetic association studies were performed to evaluate associations of LEPR genetic variants with type 2 diabetes (T2D) susceptibility.
methodsA comprehensive search was conducted to identify all eligible case-control studies for examining the associations of LEPR single nucleotide polymorphisms (SNPs) Q223R (rs1137101) and K109R (rs1137100) with T2D risk. Odds ratios (OR) and corresponding 95% confidence intervals (CIs) were used to measure the magnitudes of association.
resultsFor Q223R, 13 studies (11 articles) consisting of a total of 4030 cases and 2844 controls, and for K109R 7 studies (7 articles) consisting of 3319 cases and 2465 controls were available. Under an allele model, Q223R was not significantly associated with T2D risk (OR = 1.09, 95% CI: 0.80-1.48, P-value = 0.5989), which was consistent with results obtained under four genotypic models (ranges: ORs 1.08-1.20, 95% CIs: 0.58-2.02 to 0.64-2.26; P-values, 0.3650-0.8177, which all exceeded multiplicity-adjusted α = 0.05/5 = 0.01). In addition, no significant association was found between K109R and T2D risk based on either an allele model (OR = 0.93, 95% CI: 0.85-1.03, P-value = 0.1868) or four genotypic models (ranges: ORs 0.81-0.99, 95% CIs: 0.67-0.86 to 0.97-1.26, P-values, 0.0207-0.8804 which all exceeded multiplicity-adjusted α of 0.01). The magnitudes of association for these two SNPs were not dramatically changed in subgroup analyses by ethnicity or sensitivity analyses. Funnel plot inspections as well as Begg and Mazumdar adjusted rank correlation test and Egger linear regression test did not reveal significant publication biases in main and subgroup analyses. Bioinformatics analysis predicted that both missense SNPs were functionally neutral and benign.
conclusionsThe present meta-analysis did not detect significant genetic associations between LEPR Q223R and K109R polymorphisms and T2D risk.
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