Genetic polymorphisms of INSIG2 were associated with coronary artery disease in Uygur Chinese population in Xinjiang, China

نویسندگان

  • Dilare Adi
  • Yun Wu
  • Xiang Xie
  • Gulinaer Baituola
  • Fen Liu
  • Ying-Ying Zheng
  • Yi-Ning Yang
  • Xiao-Mei Li
  • Ding Huang
  • Xiang Ma
  • Bang-Dang Chen
  • Min-Tao Gai
  • Xiao-Cui Chen
  • Zhen-Yan Fu
  • Yi-Tong Ma
چکیده

Background: Dyslipidemia is a major and independent risk factor for the development of Coronary artery disease (CAD). The protein which is encoded by insulin induced gene2 (INSIG2) plays an important role in the mediation of the feedback control of cholesterol synthesis, lipogenesis and glucose homeostasis. The aim of the present study was to assess the association between the human INSIG2 gene and CAD in Han Chinese and Uygur Chinese population of Xinjiang, China. Methods: A total of 832 CAD patients (334 Han, 498 Uygur) and 919 controls (346 Han, 573Uygur) were selected for the present Case-control study. Three tagging SNPs (rs1261829, rs21613329 and rs17047757) of INSIG2 gene were genotyped using TaqMan® assays from Applied Biosystems following the manufacturer’s instructions and analyzed in an ABI 7900HT Fast Real-Time PCR System. Results: In the Uygur Chinese population, for total, men and women the rs17047757 was associated with CAD by analyses of a dominant model (all, P < 0.001) and the difference remained significant after multiple adjustment in a dominant model (all, P < 0.001). This relationship was also observed in rs2161829 for total and women by analyses of a recessive model (for total: P = 0.002; for women: P = 0.001, respectively) the difference remained significant after multiple adjustment in a recessive model (for both, P = 0.001). However, this relationship was not observed in this three tagging SNPs before and after multiple adjustment in Han Chinese population. Conclusion: Our results indicated that both rs17047757 and rs21613329 in the INSIG2 gene were associated with CAD in Uygur Chinese population in Xinjiang, China.

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تاریخ انتشار 2016