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  • 标题:Eleven genetic variants of seven important candidate genes involved in manifestation of type 2 diabetes mellitus
  • 本地全文:下载
  • 作者:Madhukar Saxena ; Daoud Ali ; Dinesh Raj Modi
  • 期刊名称:Journal of King Saud University - Science
  • 印刷版ISSN:1018-3647
  • 出版年度:2020
  • 卷号:32
  • 期号:5
  • 页码:2569-2575
  • DOI:10.1016/j.jksus.2020.04.014
  • 语种:English
  • 出版社:Elsevier
  • 摘要:BackgroundDiabetes especially type 2 diabetes mellitus (T2DM) is securing the rank under five around the world and leading cause of death cardiac disease and cancer. T2DM is a severe inflammatory state mainly associated to obesity and enhanced oxidative stress.ObjectivesWe have investigated eleven genetic polymorphisms of seven important genes viz. IL-10, TNF-α, IL-6, adiponectin, IL-1, IL-18, and Vitamin D-receptor. We have focused to investigate the haplotypes, gene-gene interactions and their role in determining individual susceptibility to T2DM and their manifestation.MethodsEleven genetic variants of seven important candidate genes in 440 T2DM individuals and 440 controls were genotyped using conventional polymerase chain reaction (PCR) and PCR restriction fragment length polymorphism (PCR-RFLP). All calculations were done by SPSS software and LD were analysed by haploview (SHEsis software).ResultsGenotypic frequency of rs1800872, rs1800795, rs2241766, rs17846866 and rs1946518 showed highly significant association in our population. While allele frequencies of rs1800795, rs2241766 and rs1946518 showed highly significant association. The allele set of “CGGAGGTAFTB”, “CGGAGTTAFTB” and “CGGATGTCFTB” increase the chance of diabetes up to 1.6 times. This study reflects that these individuals are more susceptible of having T2DM.ConclusionsThe present study will provide a new insight in the development and the manifestation of T2DM. These genetic studies showing gene interaction for the susceptibility of the disease may be used as prognostic markers and alter treatment strategies for T2DM.
  • 关键词:Diabetes;Gene interaction;Genetic variants;Linkage;Allele
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