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Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control
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 marro...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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SAGE Publications
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5714079/ https://www.ncbi.nlm.nih.gov/pubmed/29225483 http://dx.doi.org/10.1177/1179551417743980 |
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author | Negro, Roberto Greco, Eupremio Luigi Greco, Giacomo |
author_facet | Negro, Roberto Greco, Eupremio Luigi Greco, Giacomo |
author_sort | Negro, Roberto |
collection | PubMed |
description | 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 A(1c) (HbA(1c)): Group A—those with HbA(1c) ≤6.5% (28 patients) and Group B—those with HbA(1c) 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 HbA(1c) 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. |
format | Online Article Text |
id | pubmed-5714079 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-57140792017-12-08 Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control Negro, Roberto Greco, Eupremio Luigi Greco, Giacomo Clin Med Insights Endocrinol Diabetes Original Research 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 A(1c) (HbA(1c)): Group A—those with HbA(1c) ≤6.5% (28 patients) and Group B—those with HbA(1c) 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 HbA(1c) 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. SAGE Publications 2017-11-27 /pmc/articles/PMC5714079/ /pubmed/29225483 http://dx.doi.org/10.1177/1179551417743980 Text en © The Author(s) 2017 http://www.creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Original Research Negro, Roberto Greco, Eupremio Luigi Greco, Giacomo Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control |
title | Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control |
title_full | Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control |
title_fullStr | Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control |
title_full_unstemmed | Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control |
title_short | Active Stromal Cell–Derived Factor 1α and Endothelial Progenitor Cells are Equally Increased by Alogliptin in Good and Poor Diabetes Control |
title_sort | active stromal cell–derived factor 1α and endothelial progenitor cells are equally increased by alogliptin in good and poor diabetes control |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5714079/ https://www.ncbi.nlm.nih.gov/pubmed/29225483 http://dx.doi.org/10.1177/1179551417743980 |
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