Diagnostic Value of Serum miR-17-5p in Type 2 Diabetes Mellitus and Its Predictive Value for Chronic Complications.

Abstract

Purpose: This study aims to explore the clinical significance of miR-17-5p in T2DM and its chronic complications.

Patients and methods: A total of 100 patients with T2DM and 90 healthy controls were included. The expression of miR-17-5p was detected by reverse transcription-polymerase chain reaction. A receiver operating characteristic curve was plotted to evaluate the diagnostic value of miR-17-5p for T2DM. Pearson correlation analysis was used to explore the correlation between miR-17-5p and blood glucose indicators in T2DM patients. The Kaplan-Meier curve and multivariate Cox regression analysis were employed to analyze the factors influencing chronic complications. Liposome-mediated transfection technology was used to transfect miR-17-5p mimics and inhibitors into endothelial progenitor cells (EPCs) respectively, to achieve overexpression and knockdown of miR-17-5p in cells. On this basis, we further investigate the potential molecular mechanism by which miR-17-5p is involved in the occurrence and development of chronic complications inT2DM.

Results: Serum miR-17-5p was significantly downregulated in T2DM patients (vs healthy controls, P<0.001). The AUC for distinguishing T2DM patients from healthy individuals was 0.932. The expression of this miRNA was significantly negatively correlated with FBG (r=-0.718) and HbA1c (r=-0.695) (P<0.001). Follow-up showed that low expression of miR-17-5p was closely associated with T2DM chronic complications (complication group vs non-complication group, P<0.001), with an AUC of 0.866 for distinguishing the presence from the absence of complications. Kaplan-Meier analysis indicated that individuals with low miR-17-5p expression had a higher risk of complications (Log-rank P=0.009). Mechanistically, miR-17-5p targets FBXO48 and affects the functions of EPCs.

Conclusion: The expression of miR-17-5p is reduced in T2DM. It influences the functions of EPCs by targeting FBXO48, and may be involved in the occurrence and development of chronic complications of T2DM.