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ACTN3, Morbidity, and Healthy Aging

As human longevity increases, recent research has focused on the maintenance of optimal health during old age. One such area of focus is that of muscle function in the elderly, with a loss of muscle mass increasing the risk of negative outcomes such as sarcopenia and a decrease in bone mineral densi...

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Autores principales: Pickering, Craig, Kiely, John
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5787547/
https://www.ncbi.nlm.nih.gov/pubmed/29416549
http://dx.doi.org/10.3389/fgene.2018.00015
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author Pickering, Craig
Kiely, John
author_facet Pickering, Craig
Kiely, John
author_sort Pickering, Craig
collection PubMed
description As human longevity increases, recent research has focused on the maintenance of optimal health during old age. One such area of focus is that of muscle function in the elderly, with a loss of muscle mass increasing the risk of negative outcomes such as sarcopenia and a decrease in bone mineral density. In this mini-review, we focus on the impact of a single nucleotide polymorphism in ACTN3, shown to impact muscle phenotype in elite athletes, on loss of muscle function, maintenance of bone mineral density, and metabolic disorder risk in an elderly population. From the surveyed research, this polymorphism has a clear and demonstrable impact on muscle phenotype and bone mineral density in this population, and acts as a potential modulator for metabolic disorders. As such, knowledge of an individual’s ACTN3 genotype may better inform the management of risk factors in the elderly, as well as driving innovations in exercise program design. Subsequently, such insights may contribute to the prolonged maintenance of health and function long into old age.
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spelling pubmed-57875472018-02-07 ACTN3, Morbidity, and Healthy Aging Pickering, Craig Kiely, John Front Genet Genetics As human longevity increases, recent research has focused on the maintenance of optimal health during old age. One such area of focus is that of muscle function in the elderly, with a loss of muscle mass increasing the risk of negative outcomes such as sarcopenia and a decrease in bone mineral density. In this mini-review, we focus on the impact of a single nucleotide polymorphism in ACTN3, shown to impact muscle phenotype in elite athletes, on loss of muscle function, maintenance of bone mineral density, and metabolic disorder risk in an elderly population. From the surveyed research, this polymorphism has a clear and demonstrable impact on muscle phenotype and bone mineral density in this population, and acts as a potential modulator for metabolic disorders. As such, knowledge of an individual’s ACTN3 genotype may better inform the management of risk factors in the elderly, as well as driving innovations in exercise program design. Subsequently, such insights may contribute to the prolonged maintenance of health and function long into old age. Frontiers Media S.A. 2018-01-24 /pmc/articles/PMC5787547/ /pubmed/29416549 http://dx.doi.org/10.3389/fgene.2018.00015 Text en Copyright © 2018 Pickering and Kiely. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Pickering, Craig
Kiely, John
ACTN3, Morbidity, and Healthy Aging
title ACTN3, Morbidity, and Healthy Aging
title_full ACTN3, Morbidity, and Healthy Aging
title_fullStr ACTN3, Morbidity, and Healthy Aging
title_full_unstemmed ACTN3, Morbidity, and Healthy Aging
title_short ACTN3, Morbidity, and Healthy Aging
title_sort actn3, morbidity, and healthy aging
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5787547/
https://www.ncbi.nlm.nih.gov/pubmed/29416549
http://dx.doi.org/10.3389/fgene.2018.00015
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