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Insulin Receptor Genetic Variants Causal Association with Type 2 Diabetes: A Mendelian Randomization Study. | LitMetric

Insulin Receptor Genetic Variants Causal Association with Type 2 Diabetes: A Mendelian Randomization Study.

Curr Dev Nutr

Department of Environmental, Occupational, and Geospatial Health Sciences, The City University of New York, Graduate School of Public Health, and Health Policy, New York, NY, USA.

Published: May 2022

AI Article Synopsis

Article Abstract

Background: Type 2 diabetes (T2D) is a prevalent chronic disease associated with several comorbidities.

Objectives: This study investigated whether the risk of T2D varied with genetically predicted insulin (INS), insulin receptor (INS-R), or insulin-like growth factor 1 receptor (IGF-1R) using genetic variants in a Mendelian randomization (MR) study.

Methods: A 2-sample MR study was conducted using summary statistics from 2 genome-wide association studies (GWASs). Genetic predictors of the exposures (INS, INS-R, and IGF-1R) were obtained from a publicly available proteomics GWAS of the INTERVAL randomized controlled trial of blood donation in the United Kingdom. For T2D, the study leveraged the DIAbetes Meta-ANalysis of Trans-Ethnic association studies (DIAMANTE) consortium. The estimated associations of INS, INS-R, and IGF-1R proteins with T2D were based on independent single nucleotide polymorphisms (SNPs) strongly ( < 5 × 10) predicting each exposure. These SNPs were applied to publicly available genetic associations with T2D from the DIAMANTE case (= 74,124) and control (= 824,006) study of people of European descent. SNP-specific Wald estimates were meta-analyzed using inverse variance weighting with multiplicative random effects. Sensitivity analysis was conducted using the weighted median (WM) and MR-Egger.

Results: INS-R (based on 13 SNPs) was associated with a lower risk of T2D (OR: 0.95 per effect size; 95% CI: 0.92, 0.98; = 0.001), with similar estimates from the WM and MR-Egger. Insulin (8 SNPs) and IGF-1R (10 SNPs) were not associated with T2D. However, 1 of the SNPs for INS-R was from the blood group gene.

Conclusions: This study is consistent with a causally protective association of the INS-R with T2D. INS-R in RBCs regulates glycolysis and thus may affect their functionality and integrity. However, a pleiotropic effect via the blood group gene cannot be excluded. The INS-R may be a target for intervention by repurposing existing therapeutics or otherwise to reduce the risk of T2D.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9121804PMC
http://dx.doi.org/10.1093/cdn/nzac044DOI Listing

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