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AMPK and Exercise: Glucose Uptake and Insulin Sensitivity

AMPK is an evolutionary conserved sensor of cellular energy status that is activated during exercise. Pharmacological activation of AMPK promotes glucose uptake, fatty acid oxidation, mitochondrial biogenesis, and insulin sensitivity; processes that are reduced in obesity and contribute to the devel...

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Detalles Bibliográficos
Autor principal: O'Neill, Hayley M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Diabetes Association 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579147/
https://www.ncbi.nlm.nih.gov/pubmed/23441028
http://dx.doi.org/10.4093/dmj.2013.37.1.1
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author O'Neill, Hayley M.
author_facet O'Neill, Hayley M.
author_sort O'Neill, Hayley M.
collection PubMed
description AMPK is an evolutionary conserved sensor of cellular energy status that is activated during exercise. Pharmacological activation of AMPK promotes glucose uptake, fatty acid oxidation, mitochondrial biogenesis, and insulin sensitivity; processes that are reduced in obesity and contribute to the development of insulin resistance. AMPK deficient mouse models have been used to provide direct genetic evidence either supporting or refuting a role for AMPK in regulating these processes. Exercise promotes glucose uptake by an insulin dependent mechanism involving AMPK. Exercise is important for improving insulin sensitivity; however, it is not known if AMPK is required for these improvements. Understanding how these metabolic processes are regulated is important for the development of new strategies that target obesity-induced insulin resistance. This review will discuss the involvement of AMPK in regulating skeletal muscle metabolism (glucose uptake, glycogen synthesis, and insulin sensitivity).
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spelling pubmed-35791472013-02-25 AMPK and Exercise: Glucose Uptake and Insulin Sensitivity O'Neill, Hayley M. Diabetes Metab J Review AMPK is an evolutionary conserved sensor of cellular energy status that is activated during exercise. Pharmacological activation of AMPK promotes glucose uptake, fatty acid oxidation, mitochondrial biogenesis, and insulin sensitivity; processes that are reduced in obesity and contribute to the development of insulin resistance. AMPK deficient mouse models have been used to provide direct genetic evidence either supporting or refuting a role for AMPK in regulating these processes. Exercise promotes glucose uptake by an insulin dependent mechanism involving AMPK. Exercise is important for improving insulin sensitivity; however, it is not known if AMPK is required for these improvements. Understanding how these metabolic processes are regulated is important for the development of new strategies that target obesity-induced insulin resistance. This review will discuss the involvement of AMPK in regulating skeletal muscle metabolism (glucose uptake, glycogen synthesis, and insulin sensitivity). Korean Diabetes Association 2013-02 2013-02-15 /pmc/articles/PMC3579147/ /pubmed/23441028 http://dx.doi.org/10.4093/dmj.2013.37.1.1 Text en Copyright © 2013 Korean Diabetes Association http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
O'Neill, Hayley M.
AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
title AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
title_full AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
title_fullStr AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
title_full_unstemmed AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
title_short AMPK and Exercise: Glucose Uptake and Insulin Sensitivity
title_sort ampk and exercise: glucose uptake and insulin sensitivity
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579147/
https://www.ncbi.nlm.nih.gov/pubmed/23441028
http://dx.doi.org/10.4093/dmj.2013.37.1.1
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