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Strong relationships exist between immune factors and hyperglycemia, particularly proinflammatory factors such as interleukin (IL)-1β protein levels and genetics, which significantly correlate with the development of type 2 diabetes mellitus (T2DM). Exposure of pancreatic cells to IL-1β for an extended period enhances β-cell apoptosis, thereby affecting glucose metabolism. The study objective is to assess the functional role of IL-1β protein levels and the IL-1β rs16944 gene polymorphism in T2DM. A case-control study was conducted, involving 86 participants with T2DM and 74 controls. Blood samples were collected from the participants to assess their IL-β1 levels, fasting blood sugar levels, and fasting insulin levels. IL-1β (rs16944) was analyzed using conventional polymerase chain reaction. IL-1β rs16944 variations in the control group showed 32 (43%) of AA, 27 (36%) of AG, and 15 (20%) of GG, while T2DM patients showed 30 (35%) of AA, 34 (40%) of AG and 22 (26%) of GG variation. The logistic regression analysis showed a non-significant association between each variation and T2DM. The genome variation in patients with insulin resistance (IR) and T2DM was 8 (33%) AA, 6 (25%) AG, and 10 (42%) GG. The logistic regression test showed a non-significant association between each variation and patients with IR and T2DM. In conclusion, IL-1β levels and genetic variations of the IL-1β rs16944 gene do not affect blood sugar metabolism and I nsulin resistance in Iraqi diabetic patients.