Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?

Autores
McCarthy, Antonio Desmond; Cortizo, Ana María; Sedlinsky, Claudia
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Patients with long-term type 1 and type 2 diabetes mellitus (DM) can develop skeletal complications or “diabetic osteopathy”. These include osteopenia, osteoporosis and an increased incidence of low-stress fractures. In this context, it is important to evaluate whether current anti-diabetic treatments can secondarily affect bone metabolism. Adenosine monophosphate-activated protein kinase (AMPK) modulates multiple metabolic pathways and acts as a sensor of the cellular energy status; recent evidence suggests a critical role for AMPK in bone homeostasis. In addition, AMPK activation is believed to mediate most clinical effects of the insulin-sensitizer metformin. Over the past decade, several research groups have investigated the effects of metformin on bone, providing a considerable body of pre-clinical (in vitro, ex vivo and in vivo) as well as clinical evidence for an anabolic action of metformin on bone. However, two caveats should be kept in mind when considering metformin treatment for a patient with type 2 DM at risk for diabetic osteopathy. In the first place, met­formin should probably not be considered an anti-osteo­porotic drug; it is an insulin sensitizer with proven macrovascular benefits that can secondarily improve bone metabolism in the context of DM. Secondly, we are still awaiting the results of randomized placebo-controlled studies in humans that evaluate the effects of metformin on bone metabolism as a primary endpoint.
Facultad de Ciencias Exactas
Materia
Ciencias Exactas
Ciencias Médicas
Diabetes Mellitus
Osteoporosis
bone fractures
metformin
AMP-activated kinase
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/106633

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spelling Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?McCarthy, Antonio DesmondCortizo, Ana MaríaSedlinsky, ClaudiaCiencias ExactasCiencias MédicasDiabetes MellitusOsteoporosisbone fracturesmetforminAMP-activated kinasePatients with long-term type 1 and type 2 diabetes mellitus (DM) can develop skeletal complications or “diabetic osteopathy”. These include osteopenia, osteoporosis and an increased incidence of low-stress fractures. In this context, it is important to evaluate whether current anti-diabetic treatments can secondarily affect bone metabolism. Adenosine monophosphate-activated protein kinase (AMPK) modulates multiple metabolic pathways and acts as a sensor of the cellular energy status; recent evidence suggests a critical role for AMPK in bone homeostasis. In addition, AMPK activation is believed to mediate most clinical effects of the insulin-sensitizer metformin. Over the past decade, several research groups have investigated the effects of metformin on bone, providing a considerable body of pre-clinical (<i>in vitro</i>, <i>ex vivo</i> and <i>in vivo</i>) as well as clinical evidence for an anabolic action of metformin on bone. However, two caveats should be kept in mind when considering metformin treatment for a patient with type 2 DM at risk for diabetic osteopathy. In the first place, met­formin should probably not be considered an anti-osteo­porotic drug; it is an insulin sensitizer with proven macrovascular benefits that can secondarily improve bone metabolism in the context of DM. Secondly, we are still awaiting the results of randomized placebo-controlled studies in humans that evaluate the effects of metformin on bone metabolism as a primary endpoint.Facultad de Ciencias Exactas2016info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf122-133http://sedici.unlp.edu.ar/handle/10915/106633enginfo:eu-repo/semantics/altIdentifier/url/http://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC4807302&blobtype=pdfinfo:eu-repo/semantics/altIdentifier/url/https://www.wjgnet.com/1948-9358/full/v7/i6/122.htminfo:eu-repo/semantics/altIdentifier/issn/1948-9358info:eu-repo/semantics/altIdentifier/pmid/27022443info:eu-repo/semantics/altIdentifier/doi/10.4239/wjd.v7.i6.122info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc/4.0/Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:23:52Zoai:sedici.unlp.edu.ar:10915/106633Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:23:53.06SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
title Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
spellingShingle Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
McCarthy, Antonio Desmond
Ciencias Exactas
Ciencias Médicas
Diabetes Mellitus
Osteoporosis
bone fractures
metformin
AMP-activated kinase
title_short Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
title_full Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
title_fullStr Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
title_full_unstemmed Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
title_sort Metformin revisited: Does this regulator of AMP-activated protein kinase secondarily affect bone metabolism and prevent diabetic osteopathy?
dc.creator.none.fl_str_mv McCarthy, Antonio Desmond
Cortizo, Ana María
Sedlinsky, Claudia
author McCarthy, Antonio Desmond
author_facet McCarthy, Antonio Desmond
Cortizo, Ana María
Sedlinsky, Claudia
author_role author
author2 Cortizo, Ana María
Sedlinsky, Claudia
author2_role author
author
dc.subject.none.fl_str_mv Ciencias Exactas
Ciencias Médicas
Diabetes Mellitus
Osteoporosis
bone fractures
metformin
AMP-activated kinase
topic Ciencias Exactas
Ciencias Médicas
Diabetes Mellitus
Osteoporosis
bone fractures
metformin
AMP-activated kinase
dc.description.none.fl_txt_mv Patients with long-term type 1 and type 2 diabetes mellitus (DM) can develop skeletal complications or “diabetic osteopathy”. These include osteopenia, osteoporosis and an increased incidence of low-stress fractures. In this context, it is important to evaluate whether current anti-diabetic treatments can secondarily affect bone metabolism. Adenosine monophosphate-activated protein kinase (AMPK) modulates multiple metabolic pathways and acts as a sensor of the cellular energy status; recent evidence suggests a critical role for AMPK in bone homeostasis. In addition, AMPK activation is believed to mediate most clinical effects of the insulin-sensitizer metformin. Over the past decade, several research groups have investigated the effects of metformin on bone, providing a considerable body of pre-clinical (<i>in vitro</i>, <i>ex vivo</i> and <i>in vivo</i>) as well as clinical evidence for an anabolic action of metformin on bone. However, two caveats should be kept in mind when considering metformin treatment for a patient with type 2 DM at risk for diabetic osteopathy. In the first place, met­formin should probably not be considered an anti-osteo­porotic drug; it is an insulin sensitizer with proven macrovascular benefits that can secondarily improve bone metabolism in the context of DM. Secondly, we are still awaiting the results of randomized placebo-controlled studies in humans that evaluate the effects of metformin on bone metabolism as a primary endpoint.
Facultad de Ciencias Exactas
description Patients with long-term type 1 and type 2 diabetes mellitus (DM) can develop skeletal complications or “diabetic osteopathy”. These include osteopenia, osteoporosis and an increased incidence of low-stress fractures. In this context, it is important to evaluate whether current anti-diabetic treatments can secondarily affect bone metabolism. Adenosine monophosphate-activated protein kinase (AMPK) modulates multiple metabolic pathways and acts as a sensor of the cellular energy status; recent evidence suggests a critical role for AMPK in bone homeostasis. In addition, AMPK activation is believed to mediate most clinical effects of the insulin-sensitizer metformin. Over the past decade, several research groups have investigated the effects of metformin on bone, providing a considerable body of pre-clinical (<i>in vitro</i>, <i>ex vivo</i> and <i>in vivo</i>) as well as clinical evidence for an anabolic action of metformin on bone. However, two caveats should be kept in mind when considering metformin treatment for a patient with type 2 DM at risk for diabetic osteopathy. In the first place, met­formin should probably not be considered an anti-osteo­porotic drug; it is an insulin sensitizer with proven macrovascular benefits that can secondarily improve bone metabolism in the context of DM. Secondly, we are still awaiting the results of randomized placebo-controlled studies in humans that evaluate the effects of metformin on bone metabolism as a primary endpoint.
publishDate 2016
dc.date.none.fl_str_mv 2016
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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format article
status_str publishedVersion
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info:eu-repo/semantics/altIdentifier/url/https://www.wjgnet.com/1948-9358/full/v7/i6/122.htm
info:eu-repo/semantics/altIdentifier/issn/1948-9358
info:eu-repo/semantics/altIdentifier/pmid/27022443
info:eu-repo/semantics/altIdentifier/doi/10.4239/wjd.v7.i6.122
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc/4.0/
Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
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rights_invalid_str_mv http://creativecommons.org/licenses/by-nc/4.0/
Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
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