Background: Diabetic nephropathy is a microvascular complication that can occur in people type 2 diabetes nephropathy (T2DN). The aim of the study: To investigate the correlation between NFKB1 gene expression and NFKB1 (rs28362491) SNP with glycemic profile in Iraqi patients with diabetic nephropathy (T2DN). Materials and methods: For this study, 150 volunteers were split into three groups: 50 in the control group, 50 in the T2DM group, and 50 in the T2DN group. According to the kit's instructions, spectrophotometric analysis was used to determine the HbA1c (%) and FBG (mg/dl), blood urea (UR) and creatinine (CR) (mg/dl) parameters. The ELIAS kit was used to determine the fasting insulin (µu/ml). RT-qPCR was used for estimation of NFKB1 gene expression. Using specific primer sequences and the polymerase chain reaction method known as restriction fragment length polymorphism (PCR-RFLP), the NFKB1 (rs28362491) SNP was evaluated. Results: When compared to controls, the T2DM and T2DN groups' HbA1c%, FBG (mg/dl), INS (µu/ml), and HOMA-IR% indices of glycemic control were significantly higher (P-value<0.05), highest insulin levels, blood urea, and serum creatinine levels (P-value<0.05). For NFKB1 (rs28362491) SNP, the I/I genotype was present in 11.0% of the Control group, 21.3% of the T2DM group, and 25.8% of the T2DNP group. The p-value for this genotype was <0.001, indicating significant differences in its distribution across the groups. The results of this study revealed that there is a significant difference (P<0.001) in AFC (Average Fold Change) of NFKB1 gene expression were (1.0197±0.7), (4.448±1.08), and (8.704±2.14) in control, T2DM, and T2DN, respectively. Conclusion: Differed expression of NFKB1 between the control group and T2DN patients indicates functional involvement of NF-κB signaling in the development of DN. These results suggest that the regulatory role of NFKB1 expression and the associated effect on inflammation and renal function of T2DM need to be proven with further studies. Although this gene might serve as a potential biomarker prospect in the future, larger-scale studies are necessary for the verification of predictive susceptibility or guiding therapeutic treatments
Background: Diabetic nephropathy is a microvascular complication that can occur in people type 2 diabetes nephropathy (T2DN). The aim of the study: To investigate the correlation between NFKB1 gene expression and NFKB1 (rs28362491) SNP with glycemic profile in Iraqi patients with diabetic nephropathy (T2DN). Materials and methods: For this study, 150 volunteers were split into three groups: 50 in the control group, 50 in the T2DM group, and 50 in the T2DN group. According to the kit's instructions, spectrophotometric analysis was used to determine the HbA1c (%) and FBG (mg/dl), blood urea (UR) and creatinine (CR) (mg/dl) parameters. The ELIAS kit was used to determine the fasting insulin (µu/ml). RT-qPCR was used for estimation of NFKB1 gene expression. Using specific primer sequences and the polymerase chain reaction method known as restriction fragment length polymorphism (PCR-RFLP), the NFKB1 (rs28362491) SNP was evaluated. Results: When compared to controls, the T2DM and T2DN groups' HbA1c%, FBG (mg/dl), INS (µu/ml), and HOMA-IR% indices of glycemic control were significantly higher (P-value<0.05), highest insulin levels, blood urea, and serum creatinine levels (P-value<0.05). For NFKB1 (rs28362491) SNP, the I/I genotype was present in 11.0% of the Control group, 21.3% of the T2DM group, and 25.8% of the T2DNP group. The p-value for this genotype was <0.001, indicating significant differences in its distribution across the groups. The results of this study revealed that there is a significant difference (P<0.001) in AFC (Average Fold Change) of NFKB1 gene expression were (1.0197±0.7), (4.448±1.08), and (8.704±2.14) in control, T2DM, and T2DN, respectively. Conclusion: Differed expression of NFKB1 between the control group and T2DN patients indicates functional involvement of NF-κB signaling in the development of DN. These results suggest that the regulatory role of NFKB1 expression and the associated effect on inflammation and renal function of T2DM need to be proven with further studies. Although this gene might serve as a potential biomarker prospect in the future, larger-scale studies are necessary for the verification of predictive susceptibility or guiding therapeutic treatments