Assessment of serum adropin level in type 2 diabetic patients with or without nephropathy

Abstract

Background/aim Diabetes predisposes the affected individual to long-term macrovascular and microvascular complications. Renal complications represent a major turning point in the life of people with diabetes. Adropin is a peptide primarily secreted by the liver and brain. It is encoded by the Energy Homeostasis Associated gene (Enho). Adropin main function is to prevent insulin resistance, dyslipidemia, and impaired glucose tolerance. This study aimed to assess the serum adropin level in patients with type 2 diabetes mellitus (T2DM) and diabetic nephropathy (DN). Patients and methods This case–control study was conducted on 50 diabetic patients from Inpatient and Outpatient Clinics of Internal Medicine Department, Benha University Hospitals, Egypt, in addition to 25 apparently healthy controls. Upon their informed consent, and after complete history taking and full clinical examination, blood samples were taken for biochemical analysis and serum adropin level measurement. Adropin was measured using enzyme-linked immunosorbent assay technique. Fasting and 2-h postprandial blood glucose, glycated hemoglobin, blood urea, serum creatinine, and glomerular filtration rate were done. Results This study demonstrated that adropin shows significant reduction in the diabetic group when compared with the control group and also exhibits significant decline in the DN group when compared with the diabetic group. There was a significant negative correlation between adropin and T2DM duration as well as with glycated hemoglobin (r=−0.552 and −0.467, and P=0.001 and 0.001, respectively). Moreover, there was a significant positive correlation between adropin and estimated glomerular filtration rate (r=0.358 and P=0.002). Conclusion Adropin is significantly reduced in T2DM when compared with normal participants, and the reduction of adropin is correlated with the deterioration in kidney functions manifested by the reduction in estimated glomerular filtration rate. These findings suggested that the reduction of serum adropin may play a role in the pathogenesis of T2DM and DN.