Published online Mar 6, 2019. doi: 10.12998/wjcc.v7.i5.572
Peer-review started: November 21, 2018
First decision: December 15, 2018
Revised: December 24, 2018
Accepted: January 3, 2019
Article in press: January 3, 2019
Published online: March 6, 2019
Processing time: 106 Days and 5.5 Hours
Many biochemical mediators that are synthesized in the adipose tissue and secreted in the circulation, such as leptin, adiponectin (ADIPOQ), and resistin, are thought to be involved in obesity and insulin resistance. ADIPOQ is produced in the adipose tissue and regulates a variety of metabolic processes such as lipid metabolism, glucose and fatty acid oxidation. This hormone can reduce insulin resistance, improve lipid metabolism, and exert anti-inflammatory effects. Plasma ADIPOQ levels are decreased in patients with type 2 diabetes, metabolic syndrome, and obesity. Previous studies have shown that ADIPOQ single nucleotide polymorphisms can affect plasma ADIPOQ concentrations, which in turn affect insulin sensitivity.
Previous studies have evaluated the relationship between ADIPOQ polymorphisms and gestational diabetes mellitus (GDM), but the results of the association between ADIPOQ polymorphisms and GDM is uncertain.
We evaluated the association between ADIPOQ +45T/G, +276G/T, and -11377C/G polymorphisms and GDM with a bigger sample size and less heterogeneity. Moreover, subgroup analysis was performed by ethnicity.
Potentially related articles on human fat metabolism and GDM gene research published before October 20, 2018 were retrieved through the electronic databases EMBASE, Web of Science, PubMed, WANFANG DATA, and China National Knowledge Infrastructure. A fixed-effects or random-effects model was used to calculate pooled odds ratios (ORs) with 95% confidence intervals (CIs), based on the between-study heterogeneity to evaluate the association between AIDPOQ +45T/G, +276G/T, and -11377C/G polymorphisms and the risk of GDM.
Nine +45T/G studies included 1024 GDM cases and 1059 controls, five +276G/T studies included 590 GDM cases and 595 controls, and five -11377C/G studies included 722 GDM cases and 791 controls. Pooled ORs showed that +45T/G increased Asian GDM risk (allele model OR = 1.47, 95%CI: 1.27-1.70, P = 0.000; dominant model OR = 1.54, 95%CI: 1.27-1.85, P = 0.000; recessive mode: OR = 2.00, 95%CI: 1.43-2.85, P = 0.000), but not in South Americans (equal pattern: OR = 1.21, 95%CI: 0.68-2.41, P = 0.510; dominant model OR = 1.13, 95%CI: 0.59-2.15, P = 0.710; recessive mode OR = 2.18, 95%CI: 0.43-11.07, P = 0.350). There was no significant correlation between +276G/T (allele model OR = 0.88, 95%CI: 0.74-1.05, P = 0.158; dominant model OR = 0.91, 95%CI: 0.65-1.26, P = 0.561; recessive mode: OR = 0.82, 95%CI: 0.64-1.05, P = 0.118) or -11377C/G (equal pattern: OR = 0.96, 95%CI: 0.72-1.26, P = 0.750; dominant model OR = 1.00, 95%CI: 0.73-1.37, P = 0.980; recessive model: OR = 0.90, 95%CI: 0.61-1.32, P = 0.570) and GDM risk.
Our meta-analysis reveals the association of the ADIPOQ +45T/G polymorphism and the risk of GDM; this polymorphism increases GDM risk in Asian populations.
In order to reveal the association of ADIPOQ polymorphisms with GDM, the existence of ethnicity-specific factors, and the role that ADIPOQ polymorphisms play in pathology, studies focused on delineating ethnicity-specific factors with larger sample sizes are needed.