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
CIC Digital (CICBA)
Institución
Comisión de Investigaciones Científicas de la Provincia de Buenos Aires
OAI Identificador
oai:digital.cic.gba.gob.ar:11746/4898

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network_name_str CIC Digital (CICBA)
spelling 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
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