Research Paper Volume 10, Issue 10 pp 2935—2943

The influence of the TNFα rs1800629 polymorphism on some inflammatory biomarkers in 45-60-year-old women with metabolic syndrome

Małgorzata Szkup1, , Elżbieta Chełmecka2, , Anna Lubkowska3, , Aleksander Jerzy Owczarek2, , Elżbieta Grochans1, ,

  • 1 Department of Nursing, Pomeranian Medical University in Szczecin, Szczecin 71-210, Poland
  • 2 Department of Statistics, Department of Instrumental Analysis, School of Pharmacy with the Division of Laboratory Medicine in Sosnowiec, Medical University of Silesia, Katowice, Sosnowiec 41-200, Poland
  • 3 Department of Functional Diagnostics and Physical Medicine, Pomeranian Medical University in Szczecin, Szczecin 71-210, Poland

Received: August 18, 2018       Accepted: October 14, 2018       Published: October 31, 2018
How to Cite

Copyright: © 2018 Szkup et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Introduction: There are reports that the TNFα gene (rs1800629) can be involved in the pathogenesis of metabolic syndrome through an increased production of pro-inflammatory cytokines. Therefore, we have decided to search for the relationship between the TNFα gene polymorphisms and serum levels of proinflammatory cytokines (IL-1α, IL-1β, IL-6, TNFα, IFNγ) and CRP in women with metabolic syndrome.

Material and methods: The study sample consisted of 416 women aged 45-60 years, including 118 with metabolic syndrome. The participants were surveyed and subjected to anthropometric, biochemical and genetic analysis.

Results: We noticed that in the group meeting the criteria for metabolic syndrome, the G/G genotype of the TNFα gene was related to higher IL-6 levels than in the remainder group. The carriers of the A/G genotype in the metabolic syndrome group had significantly higher levels of IFNγ than those in the group without this syndrome. CRP was significantly higher in the group with metabolic syndrome, irrespective of the women’s genotypes.

Conclusions: The upregulation of IFNγ and IL-6 and CRP suggests that autoinflammatory process may play a significant role in the pathogenesis of metabolic syndrome. However, a direct relationship between the TNFα gene polymorphisms and inflammatory biomarkers analyzed in our study was not confirmed.


CRP: C-reactive protein; ELISA: enzyme-linked immunosorbent assai; HDL: high-density lipoprotein; IFNγ: Interferon gamma; IL-1α: Interleukin 1α; IL-1β: Interleukin 1β; IL-6: Interleukin 6; MetS: metabolic syndrome; MetS+: group included women who met the criteria for MetS according to the IDF diagnostic criteria from 2009; MetS-: women without MetS; PCR: Polymerase chain reaction; PICs: pro-inflammatory cytokines; TG: triglycerides; TNFα: tumor necrosis factor-alpha.