Abstract
Aim: To identify genetic variants in promoter areas of IL-6 -174 G>C and TNF-α -308 G>A in metabolic syndrome (Met S) and controls and associate them with Met S and serum cytokine levels.It was a cross-sectional study, including 224 cases of Met S and 200 controls. A fasting blood sample was taken and biochemical parameters including serum glucose, insulin, lipid profile, interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) were measured. Restriction fragment length polymorphism was used to identify the genetic variants of IL-6 and TNF-α. Serum levels of IL-6 and TNF-α and insulin resistance were significantly higher in cases than the controls. IL-6 showed significant positive correlation with HOMA-IR and TNF-α. CC genotype of IL-6 was associated with the increased risk of Met S (P=0.016, OR for CC vs GC+GG = 2.33, CI: 1.15–4.71). There was no significant difference of TNF-α genotypes between the cases and the controls. Serum TNF-α and IL-6 levels were significantly higher in AA and CC genotypes of TNF-α (-308 G>A) and IL-6 (-174 G>C) as compared with the GG (P=0.00 and P=0.001). Significant correlation of IL-6 with TNF-α and insulin resistance was observed that may provide us a therapeutic target for preventing metabolic derangements from insulin resistance.
Highlights
Cytokines are pleiotropic multifaceted polypeptides having versatile actions
Vicious cycle of activation of innate immunity starts resulting in the release of cytokines like interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α); these peptides establish the link between central adiposity, inflammation, insulin resistance (IR) and susceptibility to its various complications [3]
Subjects with metabolic syndrome (Met S) had significantly higher waist circumference, blood pressure (BP), serum triglyceride, glucose and insulin levels compared with the controls (P=0.00)
Summary
Cytokines are pleiotropic multifaceted polypeptides having versatile actions. The robust role of these molecules has been implicated in metabolic syndrome (Met S) and related traits. Met S named as insulin resistance syndrome (IRS) is a clustering of clinical and biochemical abnormalities such as central obesity, hypertension, impaired blood lipid and glycemic parameters. All these derangements lead to type 2 diabetes mellitus (T2DM), acute coronary syndrome (ACS), cerebrovascular accident, non-alcoholic steatohepatitis (NASH) and renal failure [1,2]. Excess body fat deposition especially perivisceral and omental adipose tissue results in an atmosphere of chronic low grade inflammation These areas are infiltrated with macrophages, lymphocytes and myeloid series suppressor cells. TNF-α generates IR by various mechanisms including serine phosphorylation of insulin receptor substrate-1 (IRS-1), altered lipid metabolism in adipocytes with increased release of License 4.0 (CC BY)
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