AGEs and bone ageing in Diabetes Mellitus
- Autores
- McCarthy, Antonio Desmond; Molinuevo, María Silvina; Cortizo, Ana María
- Año de publicación
- 2013
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión enviada
- Descripción
- Type 1 and type 2 Diabetes mellitus are associated with a decrease in bone quality that leads to an increase in low-stress fractures, a condition called diabetic osteopathy. A growing body of evidence strongly indicates that one of the main pathological mechanisms of diabetic osteopathy is an excess accumulation of advanced glycation end products (AGEs) on collagen of bone extracellular matrix. This accumulation increases exponentially during ageing, and is further increased in conditions of substrate carbonyl stress such as chronically uncompensated Diabetes mellitus. AGEs can form covalent crosslinks throughout collagen fibrils, progressively increasing bone fragility and decreasing bone post-yield strain and energy, fracture resistance and toughness. In addition, bone marrow mesenchymal cells, osteoblasts and osteoclasts express receptors such as RAGE that can bind AGEs with high affinity, altering normal cellular homeostasis. Binding of AGEs by RAGE diminishes the osteogenic potential of mesenchymal cells, inhibits osteoblastic bone-forming capacity and induces a long-term decrease in osteoclastic recruitment and bone-resorbing activity. Altogether, these cellular effects of AGEs depress bone turnover, and thus induce an even greater accumulation of AGEs. Recent in vivo, ex vivo and in vitro evidence indicates that anti-diabetic and anti-osteoporotic treatment may prevent the deleterious effects of AGEs on bone cells, providing alternative options for the pharmacological treatment of diabetic osteopathy.
- Materia
-
Ciencias Químicas
Diabetes Mellitus
Osteoporosis
Advanced glycation end products
Receptor for AGEs
Metformin
Strontium ranelate
Alendronate - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
- OAI Identificador
- oai:digital.cic.gba.gob.ar:11746/4898
Ver los metadatos del registro completo
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AGEs and bone ageing in Diabetes MellitusMcCarthy, Antonio DesmondMolinuevo, María SilvinaCortizo, Ana MaríaCiencias QuímicasDiabetes MellitusOsteoporosisAdvanced glycation end productsReceptor for AGEsMetforminStrontium ranelateAlendronateType 1 and type 2 Diabetes mellitus are associated with a decrease in bone quality that leads to an increase in low-stress fractures, a condition called diabetic osteopathy. A growing body of evidence strongly indicates that one of the main pathological mechanisms of diabetic osteopathy is an excess accumulation of advanced glycation end products (AGEs) on collagen of bone extracellular matrix. This accumulation increases exponentially during ageing, and is further increased in conditions of substrate carbonyl stress such as chronically uncompensated Diabetes mellitus. AGEs can form covalent crosslinks throughout collagen fibrils, progressively increasing bone fragility and decreasing bone post-yield strain and energy, fracture resistance and toughness. In addition, bone marrow mesenchymal cells, osteoblasts and osteoclasts express receptors such as RAGE that can bind AGEs with high affinity, altering normal cellular homeostasis. Binding of AGEs by RAGE diminishes the osteogenic potential of mesenchymal cells, inhibits osteoblastic bone-forming capacity and induces a long-term decrease in osteoclastic recruitment and bone-resorbing activity. Altogether, these cellular effects of AGEs depress bone turnover, and thus induce an even greater accumulation of AGEs. Recent in vivo, ex vivo and in vitro evidence indicates that anti-diabetic and anti-osteoporotic treatment may prevent the deleterious effects of AGEs on bone cells, providing alternative options for the pharmacological treatment of diabetic osteopathy.2013info:eu-repo/semantics/articleinfo:eu-repo/semantics/submittedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfhttps://digital.cic.gba.gob.ar/handle/11746/4898enginfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/reponame:CIC Digital (CICBA)instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Airesinstacron:CICBA2025-09-29T13:40:06Zoai:digital.cic.gba.gob.ar:11746/4898Institucionalhttp://digital.cic.gba.gob.arOrganismo científico-tecnológicoNo correspondehttp://digital.cic.gba.gob.ar/oai/snrdmarisa.degiusti@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:94412025-09-29 13:40:06.214CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Airesfalse |
dc.title.none.fl_str_mv |
AGEs and bone ageing in Diabetes Mellitus |
title |
AGEs and bone ageing in Diabetes Mellitus |
spellingShingle |
AGEs and bone ageing in Diabetes Mellitus McCarthy, Antonio Desmond Ciencias Químicas Diabetes Mellitus Osteoporosis Advanced glycation end products Receptor for AGEs Metformin Strontium ranelate Alendronate |
title_short |
AGEs and bone ageing in Diabetes Mellitus |
title_full |
AGEs and bone ageing in Diabetes Mellitus |
title_fullStr |
AGEs and bone ageing in Diabetes Mellitus |
title_full_unstemmed |
AGEs and bone ageing in Diabetes Mellitus |
title_sort |
AGEs and bone ageing in Diabetes Mellitus |
dc.creator.none.fl_str_mv |
McCarthy, Antonio Desmond Molinuevo, María Silvina Cortizo, Ana María |
author |
McCarthy, Antonio Desmond |
author_facet |
McCarthy, Antonio Desmond Molinuevo, María Silvina Cortizo, Ana María |
author_role |
author |
author2 |
Molinuevo, María Silvina Cortizo, Ana María |
author2_role |
author author |
dc.subject.none.fl_str_mv |
Ciencias Químicas Diabetes Mellitus Osteoporosis Advanced glycation end products Receptor for AGEs Metformin Strontium ranelate Alendronate |
topic |
Ciencias Químicas Diabetes Mellitus Osteoporosis Advanced glycation end products Receptor for AGEs Metformin Strontium ranelate Alendronate |
dc.description.none.fl_txt_mv |
Type 1 and type 2 Diabetes mellitus are associated with a decrease in bone quality that leads to an increase in low-stress fractures, a condition called diabetic osteopathy. A growing body of evidence strongly indicates that one of the main pathological mechanisms of diabetic osteopathy is an excess accumulation of advanced glycation end products (AGEs) on collagen of bone extracellular matrix. This accumulation increases exponentially during ageing, and is further increased in conditions of substrate carbonyl stress such as chronically uncompensated Diabetes mellitus. AGEs can form covalent crosslinks throughout collagen fibrils, progressively increasing bone fragility and decreasing bone post-yield strain and energy, fracture resistance and toughness. In addition, bone marrow mesenchymal cells, osteoblasts and osteoclasts express receptors such as RAGE that can bind AGEs with high affinity, altering normal cellular homeostasis. Binding of AGEs by RAGE diminishes the osteogenic potential of mesenchymal cells, inhibits osteoblastic bone-forming capacity and induces a long-term decrease in osteoclastic recruitment and bone-resorbing activity. Altogether, these cellular effects of AGEs depress bone turnover, and thus induce an even greater accumulation of AGEs. Recent in vivo, ex vivo and in vitro evidence indicates that anti-diabetic and anti-osteoporotic treatment may prevent the deleterious effects of AGEs on bone cells, providing alternative options for the pharmacological treatment of diabetic osteopathy. |
description |
Type 1 and type 2 Diabetes mellitus are associated with a decrease in bone quality that leads to an increase in low-stress fractures, a condition called diabetic osteopathy. A growing body of evidence strongly indicates that one of the main pathological mechanisms of diabetic osteopathy is an excess accumulation of advanced glycation end products (AGEs) on collagen of bone extracellular matrix. This accumulation increases exponentially during ageing, and is further increased in conditions of substrate carbonyl stress such as chronically uncompensated Diabetes mellitus. AGEs can form covalent crosslinks throughout collagen fibrils, progressively increasing bone fragility and decreasing bone post-yield strain and energy, fracture resistance and toughness. In addition, bone marrow mesenchymal cells, osteoblasts and osteoclasts express receptors such as RAGE that can bind AGEs with high affinity, altering normal cellular homeostasis. Binding of AGEs by RAGE diminishes the osteogenic potential of mesenchymal cells, inhibits osteoblastic bone-forming capacity and induces a long-term decrease in osteoclastic recruitment and bone-resorbing activity. Altogether, these cellular effects of AGEs depress bone turnover, and thus induce an even greater accumulation of AGEs. Recent in vivo, ex vivo and in vitro evidence indicates that anti-diabetic and anti-osteoporotic treatment may prevent the deleterious effects of AGEs on bone cells, providing alternative options for the pharmacological treatment of diabetic osteopathy. |
publishDate |
2013 |
dc.date.none.fl_str_mv |
2013 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/submittedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
submittedVersion |
dc.identifier.none.fl_str_mv |
https://digital.cic.gba.gob.ar/handle/11746/4898 |
url |
https://digital.cic.gba.gob.ar/handle/11746/4898 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ |
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openAccess |
rights_invalid_str_mv |
http://creativecommons.org/licenses/by/4.0/ |
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application/pdf |
dc.source.none.fl_str_mv |
reponame:CIC Digital (CICBA) instname:Comisión de Investigaciones Científicas de la Provincia de Buenos Aires instacron:CICBA |
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CIC Digital (CICBA) |
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CIC Digital (CICBA) |
instname_str |
Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
instacron_str |
CICBA |
institution |
CICBA |
repository.name.fl_str_mv |
CIC Digital (CICBA) - Comisión de Investigaciones Científicas de la Provincia de Buenos Aires |
repository.mail.fl_str_mv |
marisa.degiusti@sedici.unlp.edu.ar |
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