| dc.creator | Tolosa, María José Anahí | |
| dc.creator | Chuguransky, Sara Rocío | |
| dc.creator | Sedlinsky, Claudia | |
| dc.creator | Schurman, León | |
| dc.creator | McCarthy, Antonio Desmond | |
| dc.creator | Molinuevo, María Silvina | |
| dc.creator | Cortizo, Ana María | |
| dc.date | 2013-06 | |
| dc.date | 2022-02-08T14:44:21Z | |
| dc.date.accessioned | 2023-07-15T05:00:53Z | |
| dc.date.available | 2023-07-15T05:00:53Z | |
| dc.identifier | http://sedici.unlp.edu.ar/handle/10915/130692 | |
| dc.identifier | issn:1872-8227 | |
| dc.identifier | issn:0168-8227 | |
| dc.identifier.uri | https://repositorioslatinoamericanos.uchile.cl/handle/2250/7471756 | |
| dc.description | Aims: Diabetes mellitus is associated with metabolic bone disease and increased lowimpact fractures. The insulin-sensitizer metformin possesses in vitro, in vivo and ex vivo osteogenic effects, although this has not been adequately studied in the context of diabetes. We evaluated the effect of insulin-deficient diabetes and/or metformin on bone microarchitecture, on osteogenic potential of bone marrow progenitor cells (BMPC) and possible mechanisms involved.
Methods: Partially insulin-deficient diabetes was induced in rats by nicotinamide/streptozotocin-injection, with or without oral metformin treatment. Femoral metaphysis microarchitecture, ex vivo osteogenic potential of BMPC, and BMPC expression of Runx-2, PPARg and receptor for advanced glycation endproducts (RAGE) were investigated.
Results: Histomorphometric analysis of diabetic femoral metaphysis demonstrated a slight decrease in trabecular area and a significant reduction in osteocyte density, growth plate height and TRAP (tartrate-resistant acid phosphatase) activity in the primary spongiosa. BMPC obtained from diabetic animals showed a reduction in Runx-2/PPARg ratio and in their osteogenic potential, and an increase in RAGE expression. Metformin treatment prevented the diabetes-induced alterations in bone micro-architecture and BMPC osteogenic potential.
Conclusion: Partially insulin-deficient diabetes induces deleterious effects on long-bone micro-architecture that are associated with a decrease in BMPC osteogenic potential, which could be mediated by a decrease in their Runx-2/PPARg ratio and up-regulation of RAGE. These diabetes-induced alterations can be totally or partially prevented by oral administration of metformin. | |
| dc.description | Facultad de Ciencias Exactas | |
| dc.description | Laboratorio de Investigación en Osteopatías y Metabolismo Mineral | |
| dc.format | application/pdf | |
| dc.format | 177-186 | |
| dc.language | en | |
| dc.rights | http://creativecommons.org/licenses/by-nc-sa/4.0/ | |
| dc.rights | Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) | |
| dc.subject | Ciencias Exactas | |
| dc.subject | Biología | |
| dc.subject | Diabetes Mellitus | |
| dc.subject | Metformin | |
| dc.subject | Bone microarchitecture | |
| dc.subject | Bone marrow progenitor cells | |
| dc.title | Insulin-deficient diabetes-induced bone microarchitecture alterations are associated with a decrease in the osteogenic potential of bone marrow progenitor cells: Preventive effects of metformin | |
| dc.type | Articulo | |
| dc.type | Articulo | |
