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Increasing muscle mass to improve metabolism

Skeletal muscle insulin resistance is a predictor of the development of type 2 diabetes and maintenance of adequate muscle glucose disposal in muscle may help to prevent diabetes. Lipodystrophy is a type of diabetes caused by a reduction of white adipose tissue and the adipokine leptin. Lipidemia, i...

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Detalles Bibliográficos
Autores principales: McPherron, Alexandra C., Guo, Tingqing, Bond, Nichole D., Gavrilova, Oksana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661116/
https://www.ncbi.nlm.nih.gov/pubmed/23805405
http://dx.doi.org/10.4161/adip.22500
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author McPherron, Alexandra C.
Guo, Tingqing
Bond, Nichole D.
Gavrilova, Oksana
author_facet McPherron, Alexandra C.
Guo, Tingqing
Bond, Nichole D.
Gavrilova, Oksana
author_sort McPherron, Alexandra C.
collection PubMed
description Skeletal muscle insulin resistance is a predictor of the development of type 2 diabetes and maintenance of adequate muscle glucose disposal in muscle may help to prevent diabetes. Lipodystrophy is a type of diabetes caused by a reduction of white adipose tissue and the adipokine leptin. Lipidemia, insulin resistance and hyperphagia develop as a consequence. In a recent study, we showed that increasing skeletal muscle mass by inhibiting signaling of myostatin, a transforming growth factor β (TGFβ) family member that negatively regulates muscle growth, prevents the development of diabetes in a mouse model of lipodystrophy. Muscle-specific myostatin inhibition also prevented hyperphagia suggesting muscle may regulate food intake. Here we discuss these results in the context of strategies to increase muscle insulin sensitivity as well as new findings about the effects of myostatin and other TGFβ family members on similar metabolic processes.
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spelling pubmed-36611162013-06-26 Increasing muscle mass to improve metabolism McPherron, Alexandra C. Guo, Tingqing Bond, Nichole D. Gavrilova, Oksana Adipocyte Commentary Skeletal muscle insulin resistance is a predictor of the development of type 2 diabetes and maintenance of adequate muscle glucose disposal in muscle may help to prevent diabetes. Lipodystrophy is a type of diabetes caused by a reduction of white adipose tissue and the adipokine leptin. Lipidemia, insulin resistance and hyperphagia develop as a consequence. In a recent study, we showed that increasing skeletal muscle mass by inhibiting signaling of myostatin, a transforming growth factor β (TGFβ) family member that negatively regulates muscle growth, prevents the development of diabetes in a mouse model of lipodystrophy. Muscle-specific myostatin inhibition also prevented hyperphagia suggesting muscle may regulate food intake. Here we discuss these results in the context of strategies to increase muscle insulin sensitivity as well as new findings about the effects of myostatin and other TGFβ family members on similar metabolic processes. Landes Bioscience 2013-04-01 2013-04-01 /pmc/articles/PMC3661116/ /pubmed/23805405 http://dx.doi.org/10.4161/adip.22500 Text en Copyright © 2013 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Commentary
McPherron, Alexandra C.
Guo, Tingqing
Bond, Nichole D.
Gavrilova, Oksana
Increasing muscle mass to improve metabolism
title Increasing muscle mass to improve metabolism
title_full Increasing muscle mass to improve metabolism
title_fullStr Increasing muscle mass to improve metabolism
title_full_unstemmed Increasing muscle mass to improve metabolism
title_short Increasing muscle mass to improve metabolism
title_sort increasing muscle mass to improve metabolism
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661116/
https://www.ncbi.nlm.nih.gov/pubmed/23805405
http://dx.doi.org/10.4161/adip.22500
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