Potential associations between variants of genes encoding regulators of inflammation, and mediators of inflammation in type 2 diabetes and insulin resistance.

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Ozbayer C., Kebapci M. N., Kurt H., Colak E., Gunes H. V., Degirmenci I.

Journal of clinical pharmacy and therapeutics, vol.46, pp.1395-1403, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 46
  • Publication Date: 2021
  • Doi Number: 10.1111/jcpt.13471
  • Journal Name: Journal of clinical pharmacy and therapeutics
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, CINAHL, EMBASE, International Pharmaceutical Abstracts, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.1395-1403
  • Keywords: genetic variations, insulin Resistance, IRAK4, MyD88, TRAF6, type 2 diabetes, SIGNALING PATHWAY, IKK-BETA, KINASE 4, POLYMORPHISMS, MYD88, TLR4, CYCLOOXYGENASE-2, SUSCEPTIBILITY, CONSEQUENCES, NEPHROPATHY
  • Eskisehir Osmangazi University Affiliated: Yes

Abstract

What is known and objective Type 2 diabetes (T2DM) is a multigenic disease that develops with impaired beta-cell function and insulin sensitivity and has a high prevalence worldwide. A cause often postulated for type 2 diabetes is chronic inflammation. It has been suggested that inflammatory regulators can inhibit insulin signal transduction and that inflammation is involved in insulin resistance (IR) and the pathogenesis of type 2 diabetes. In this direction, we aimed to investigate the gene variants of MyD88 (rs1319438, rs199396), IRAK4 (rs1461567, rs4251513, rs4251559) and TRAF6 (rs331455, rs331457) and serum levels of COX-2, NF-kappa B, iNOS in T2DM and IR.