Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control. (25th November 2017)

• Record Type: Journal Article
• Authors: Negro, Roberto; Greco, Eupremio Luigi; Greco, Giacomo
• Is Part Of: Clinical medicine insights. Volume 10(2017)
• Publication Date: 2017-11-25
• Subjects: Diabetes -- DPP-4 inhibitors -- endothelial progenitor cells -- alogliptin -- SDF-1α -- metformin; Endocrinology -- Periodicals; Diabetes -- Periodicals; Endocrinology; Diabetes Mellitus; Diabetes; Endocrinology; Electronic journals; Periodicals; Fulltext; Internet Resources; Periodicals; Periodicals; 616.4005
• DOI: 10.1177/1179551417743980
• Languages: English
• ISSNs: 1179-5514

Abstract

Background: It is postulated that the ability of dipeptidyl peptidase-4 inhibitors (DPP-4-i) to increase circulating endothelial progenitor cells (EPCs) may be at least partly mediated by active stromal cell–derived factor 1α (SDF-1α) (a pivotal mediator of stem cell mobilization from the bone marrow). As other DPP-4-i were demonstrated to increase EPC concentrations, in this study, we sought to investigate the ability of the DPP-4-i alogliptin in modifying EPCs and SDF-1α, in patients with good and poor diabetes control. Methods: Two groups of diabetic patients on metformin were divided by hemoglobin A1c (HbA1c ): Group A—those with HbA1c ≤6.5% (28 patients) and Group B—those with HbA1c 7.5% to 8.5% (31 patients). Both groups received alogliptin 25 mg/daily for 4 months. At baseline and 4 months later, clinical, laboratory parameters, EPCs, and active SDF-1α were determined. Results: After 4-month treatment with alogliptin, either Group A or Group B showed reduced HbA1c levels and concomitant similar increase in EPCs and active SDF-1α. Conclusions: Alogliptin showed significant benefits in increasing EPCs and active SDF-1α either in good or poor diabetes control. The study demonstrated that similar to other DPP-4-i, also alogliptin is able to increase EPC concentrations, suggesting the existence of a class effect mediated by SDF-1α. The extent of increase in EPCs is independent from baseline diabetes control.