Prediction of Protein Kinase A with Type 2 Diabetes Mellitus and Its Relation with Insulin and Homeostasis Model Assessment Insulin Resistance in Najaf Patients
Abstract Background: In the world, chronic disease represents the predominant illness. Autoimmune disease, β-cell dysfunction, and obesity are the main causes of type 2 diabetes mellitus (T2DM). The signal transducer for several external stimuli, which acts as a second messenger, is protein kinase A (PKA). It is accompanied by disease and controls several biological processes. Objectives: To study the amount of PKA in diabetic mellitus type 2 and its correlation with insulin and homeostasis model assessment insulin resistance (HOMA-IR) in Najaf patients province. Materials and Methods: In total, 120 subjects, 60 diagnosed with chronic diabetes mellitus type 2, and 60 healthy subjects were enrolled in the current study. Age ranged between 35 and 60 years for patients and healthy. PKA and insulin levels in serum were estimated by enzyme-linked immunosorbent assay technique, while HOMA-IR was calculated by the Tjokroprawiro method. Results: In T2DM, serum PKA levels significantly decreased in patients compared with control group ( P < 0.001). On the other hand, this study observed a significant ( P value < 0.001) negative, weak correlation for PKA with insulin and nonsignificant ( P value > 0.05) no correlation with HOMA-IR in DM patients. Conclusion: Among T2DM patients in Najaf province, a decrease in the level of PKA, insulin, and HOMA-IR in patients; indicates a significant link with the progression of chronic T2DM.
Authors
- Moaed E. Al‐Gazally (ORCID: https://orcid.org/0000-0002-5325-5280)
- Ali AL Bayati
- Thualfaqqar Kamil Yousef
Institutions
- University of Babylon (IQ)
- University of Alkafeel (IQ)
- Directorate of Health (IS)
- University of Kufa (IQ)
Publication Details
- Journal
- Medical Journal of Babylon
- Published
- 2025-10-01
- DOI
- https://doi.org/10.4103/mjbl.mjbl_369_23
- Primary Topic
- Metabolism, Diabetes, and Cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.00