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Association of Interleukin-6 Polymorphisms With Obesity: A Systematic Review and Meta-Analysis Publisher Pubmed



Gholami M1, 2 ; Sharifi F3 ; Shahriari S4 ; Khoshnevisan K5 ; Larijani B2 ; Amoli MM4
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Authors Affiliations
  1. 1. Obesity and Eating Habits Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Endocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Elderly Health Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Metabolic Disorders Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Biosensor Research Center, Endocrinology and Metabolism Molecular-Cellular Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran

Source: Cytokine Published:2019


Abstract

Obesity is a common metabolic disorder with increasing trend all around the world. Owing to the role of pro-inflammatory cytokines on obesity, we aimed to investigate the role of interleukin-6 (IL-6) polymorphisms on risk of obesity. Electronic literatures were searched in Web of Science, PubMed, Embase, and Scopus. The references of relevant reviews and included studies were also manually checked. All types of observational studies from 1 January 1992 to 28 February 2018 were included. Odds ratio (OR) was estimated by fixed and random effect model. Subgroup analysis was carried out based on age statues. Pooling analysis of eligible studies have been considered for rs2069845 and rs1800796, and no significant results were observed. Minor allele of IL-6 rs1800797polymorphism decreased the risk of obesity/overweight in allelic 0.74 (0.59–0.92), dominant 0.65 (0.49–0.85), and over-dominant 0.66 (0.51–0.87) models. Fourteen eligible studies were included for rs1800795. According to BMI, C allele showed increased risk of obesity in genetic models containing homozygote model 1.47 (1.02–2.12) for body mass index (BMI) ≥ 25 vs. BMI < 25, recessive model 1.32 (1.07–1.63) for BMI ≥ 30 vs. BMI < 25, and homozygote model 1.35 (1.10–1.66) for BMI ≥ 30 vs. BMI < 30. In overall definition of obesity more significant results were observed, including homozygote model in obese vs. normal 1.71 (1.14–2.56). Similarly, subgroups analysis revealed additional significant results. Minor alleles of rs1800795 raised and rs1800797 reduced the risk of obesity, while rs1800796 and rs2069845 may not be associated. However, more observational studies are recommended to confirm these results. © 2019 Elsevier Ltd
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