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Regulation of exercise-stimulated glucose uptake in skeletal muscle

AMP-activated protein kinase (AMPK) is a Ser/Thr kinase that has been thought to be an important mediator for exercise-stimulated glucose uptake in skeletal muscle. Liver kinase B1 (LKB1) is an upstream kinase for AMPK and AMPK-related protein kinases, of which the function in skeletal muscle has no...

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Autor principal: Koh, Ho-Jin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Pediatric Endocrinology 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960015/
https://www.ncbi.nlm.nih.gov/pubmed/27462580
http://dx.doi.org/10.6065/apem.2016.21.2.61
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author Koh, Ho-Jin
author_facet Koh, Ho-Jin
author_sort Koh, Ho-Jin
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description AMP-activated protein kinase (AMPK) is a Ser/Thr kinase that has been thought to be an important mediator for exercise-stimulated glucose uptake in skeletal muscle. Liver kinase B1 (LKB1) is an upstream kinase for AMPK and AMPK-related protein kinases, of which the function in skeletal muscle has not been well documented. Our group and others have generated mice lacking AMPK activity in skeletal muscle, as well as muscle-specific LKB1 knockout mice. In this review, we discuss the potential role of AMPK and LKB1 in regulating exercise-stimulated glucose uptake in skeletal muscle. We also discuss our recent study, demonstrating the molecular mechanism of obesity-induced development of skeletal muscle insulin resistance.
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spelling pubmed-49600152016-07-26 Regulation of exercise-stimulated glucose uptake in skeletal muscle Koh, Ho-Jin Ann Pediatr Endocrinol Metab Review Article AMP-activated protein kinase (AMPK) is a Ser/Thr kinase that has been thought to be an important mediator for exercise-stimulated glucose uptake in skeletal muscle. Liver kinase B1 (LKB1) is an upstream kinase for AMPK and AMPK-related protein kinases, of which the function in skeletal muscle has not been well documented. Our group and others have generated mice lacking AMPK activity in skeletal muscle, as well as muscle-specific LKB1 knockout mice. In this review, we discuss the potential role of AMPK and LKB1 in regulating exercise-stimulated glucose uptake in skeletal muscle. We also discuss our recent study, demonstrating the molecular mechanism of obesity-induced development of skeletal muscle insulin resistance. The Korean Society of Pediatric Endocrinology 2016-06 2016-06-30 /pmc/articles/PMC4960015/ /pubmed/27462580 http://dx.doi.org/10.6065/apem.2016.21.2.61 Text en © 2016 Annals of Pediatric Endocrinology & Metabolism http://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Koh, Ho-Jin
Regulation of exercise-stimulated glucose uptake in skeletal muscle
title Regulation of exercise-stimulated glucose uptake in skeletal muscle
title_full Regulation of exercise-stimulated glucose uptake in skeletal muscle
title_fullStr Regulation of exercise-stimulated glucose uptake in skeletal muscle
title_full_unstemmed Regulation of exercise-stimulated glucose uptake in skeletal muscle
title_short Regulation of exercise-stimulated glucose uptake in skeletal muscle
title_sort regulation of exercise-stimulated glucose uptake in skeletal muscle
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4960015/
https://www.ncbi.nlm.nih.gov/pubmed/27462580
http://dx.doi.org/10.6065/apem.2016.21.2.61
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