Inflammatory Markers and Haptoglobin Polymorphism in Saudi with Non-insulin-dependent Diabetes Mellitus

نویسندگان

  • Abdelmarouf Mohieldein
  • Mohammad Alzohairy
  • Marghoob Hasan
  • Amjad A. Khan
چکیده

OBJECTIVES Haptoglobin (Hp) polymorphism associated with clinical evolution of several inflammatory diseases and considered as a predictive factor for development of diabetes complications. We designed the present study to investigate the frequency distribution of Hp phenotypes among Saudi with non-insulin-dependent diabetes mellitus compared to healthy nondiabetic subjects. Moreover, we explored the possibility of relationship between serum levels of inflammatory markers (namely, high-sensitive C-reactive proteins "hs-CRP", interleukin (IL)-6, and Hp) and Hp phenotypes. METHODS In the present case-control study, we enrolled 60 type 2 diabetic patients as the study group and 60 healthy subjects as the control group. We assayed serum levels of Hp and hs-CRP by immunoturbidimetric method; while IL-6 was measured by ELISA. Native polyacrylamide gel electrophoresis was used for determination of Hp phenotypes. RESULTS In type 2 diabetics, serum concentrations of IL-6, hs-CRP, and Hp were significantly elevated and correlated to body mass index. Moreover, there was a significant correlation between plasma glucose level and Hp (r = 0.577, p = 0.000), IL-6 (r = 0.448, p = 0.000), and hs-CRP (r = 0.380, p = 0.001). In addition, data demonstrated a positive correlation between HbA1c and Hp (r = 0.521, p = 0.000), IL-6 (r = 0.420, p = 0.001), and hs-CRP (r = 0.353, p = 0.008). Hp 2-1 phenotype predominated among subjects in both study and control groups. No significant association between Hp phenotypes with any of the investigated inflammatory markers was documented. CONCLUSION Inflammation may represent the link between type 2 diabetes and obesity. Hp 2-1 was the predominant phenotype among Saudi type 2 diabetics as well as healthy subjects. In addition to Hp; other possible genetic polymorphisms like CRP may have its effect on diabetes through different mechanisms.

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عنوان ژورنال:

دوره 5  شماره 

صفحات  -

تاریخ انتشار 2012