AGEs and Bone Ageing in Diabetes Mellitus
- Autores
- McCarthy, Antonio Desmond; Molinuevo, Maria Silvina; Cortizo, Ana María
- Año de publicación
- 2013
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- 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.
Fil: McCarthy, Antonio Desmond. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Molinuevo, Maria Silvina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Cortizo, Ana María. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina - Materia
-
Diabetes mellitus
Advanced glycation end products
Osteoporosis
Receptor for AGEs
Metformin
Strontium ranelate
Alendronate - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/23677
Ver los metadatos del registro completo
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AGEs and Bone Ageing in Diabetes MellitusMcCarthy, Antonio DesmondMolinuevo, Maria SilvinaCortizo, Ana MaríaDiabetes mellitusAdvanced glycation end productsOsteoporosisReceptor for AGEsMetforminStrontium ranelateAlendronatehttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Type 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.Fil: McCarthy, Antonio Desmond. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Molinuevo, Maria Silvina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Cortizo, Ana María. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaOMICS International2013-07info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/23677McCarthy, Antonio Desmond; Molinuevo, Maria Silvina; Cortizo, Ana María; AGEs and Bone Ageing in Diabetes Mellitus; OMICS International; Journal of Diabetes and Metabolism; 4; 6; 7-2013; 1-8; 10002762155-6156CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.4172/2155-6156.1000276info:eu-repo/semantics/altIdentifier/url/https://www.omicsonline.org/2155-6156/2155-6156-4-276.php?aid=16560info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:16:41Zoai:ri.conicet.gov.ar:11336/23677instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:16:41.341CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
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 Diabetes mellitus Advanced glycation end products Osteoporosis 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, Maria Silvina Cortizo, Ana María |
author |
McCarthy, Antonio Desmond |
author_facet |
McCarthy, Antonio Desmond Molinuevo, Maria Silvina Cortizo, Ana María |
author_role |
author |
author2 |
Molinuevo, Maria Silvina Cortizo, Ana María |
author2_role |
author author |
dc.subject.none.fl_str_mv |
Diabetes mellitus Advanced glycation end products Osteoporosis Receptor for AGEs Metformin Strontium ranelate Alendronate |
topic |
Diabetes mellitus Advanced glycation end products Osteoporosis Receptor for AGEs Metformin Strontium ranelate Alendronate |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.2 https://purl.org/becyt/ford/3 |
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. Fil: McCarthy, Antonio Desmond. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Molinuevo, Maria Silvina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Cortizo, Ana María. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina |
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 |
2013-07 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/23677 McCarthy, Antonio Desmond; Molinuevo, Maria Silvina; Cortizo, Ana María; AGEs and Bone Ageing in Diabetes Mellitus; OMICS International; Journal of Diabetes and Metabolism; 4; 6; 7-2013; 1-8; 1000276 2155-6156 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/23677 |
identifier_str_mv |
McCarthy, Antonio Desmond; Molinuevo, Maria Silvina; Cortizo, Ana María; AGEs and Bone Ageing in Diabetes Mellitus; OMICS International; Journal of Diabetes and Metabolism; 4; 6; 7-2013; 1-8; 1000276 2155-6156 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.4172/2155-6156.1000276 info:eu-repo/semantics/altIdentifier/url/https://www.omicsonline.org/2155-6156/2155-6156-4-276.php?aid=16560 |
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info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
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application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
OMICS International |
publisher.none.fl_str_mv |
OMICS International |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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