Abstract
Type 2 diabetes mellitus (T2DM) is a metabolic disease and cytokines show a vital role in the T2DM progress. The goal of this research was to assess serum levels of tumor necrosis factor-alpha (TNF-?) and interferon-gamma (IFN-?) gene polymorphism in T2DM in Kurdish patients. Levels of serum IFN-? and TNF-? were assessed through enzyme-linked immune sorbent assay in individuals with T2DM and the control group. DNA was extracted and the amplification refractory mutational system method was utilized for genotyping the IFN-? (+874) A/T and TNF-? (-308) G/A. The Hardy-Weinberg equilibrium was evaluated with the ?2-test. The IFN- ? serum levels were significantly different between patients with T2DM and control individuals (P<0.05). But the C-reactive protein (CRP) and TNF-? serum levels were not significantly different between them (P>0.05). The serum level of IFN- ? (+874) AT genotype and TNF-? (- 308) GG genotypes were significantly higher in the T2DM group comparing with healthy people (P<0.05). A significant relation between T2DM and IFN-? (+874) gene polymorphism's TT and AT genotypes was observed. Also, it was not a significant relation between TNF-? (?308) gene polymorphism's GG and GA genotypes and T2DM. But the statistically significant difference was found in the genotype AA frequency. Genetic polymorphisms of IFN-? (+874) and TNF-? (?308) are contributed to the genetic susceptibility for T2DM development in the Kurdish population. Early screening of these two genetic polymorphisms may assist in the early control and management of T2DM.
Highlights
Defects in insulin action can result in impaired glucose metabolism that causes chronic metabolic disease, type 2 diabetes mellitus (T2DM) [1]
At the early stages of Type 2 diabetes mellitus (T2DM), these proteins appear, their concentrations enhance with developing the disease [8]
It was demonstrated that pro-inflammatory cytokines, immune system activation, and inflammation have a crucial effect on the progress and pathogenesis of T2DM [21, 22]
Summary
Defects in insulin action can result in impaired glucose metabolism that causes chronic metabolic disease, type 2 diabetes mellitus (T2DM) [1]. It has been recognized that cytokines have a crucial effect on T2DM They regulate immune response and different factors affect the cytokine expression via immune cells. Some of these factors are hormonal conditions, inflammation, infection and gene polymorphisms [5]. The effect of genetic polymorphism on pro-inflammatory and anti-inflammatory specific cytokine genes is a regular risk factor for diabetes development [6, 7]. Enhancing levels of these pro-inflammatory cytokines result in hepatic secretion and production of proteins like amyloid-A, plasminogen activator inhibitor, and C-reactive protein (CRP). At the early stages of T2DM, these proteins appear, their concentrations enhance with developing the disease [8]
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