| Signaling mechanisms in skeletal muscle: acute responses and chronic adaptations to exercise. | |
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MedLine Citation:
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PMID: 18380005 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Physical activity elicits physiological responses in skeletal muscle that result in a number of health benefits, in particular in disease states, such as type 2 diabetes. An acute bout of exercise/muscle contraction improves glucose homeostasis by increasing skeletal muscle glucose uptake, while chronic exercise training induces alterations in the expression of metabolic genes, such as those involved in muscle fiber type, mitochondrial biogenesis, or glucose transporter 4 (GLUT4) protein levels. A primary goal of exercise research is to elucidate the mechanisms that regulate these important metabolic and transcriptional events in skeletal muscle. In this review, we briefly summarize the current literature describing the molecular signals underlying skeletal muscle responses to acute and chronic exercise. The search for possible exercise/contraction-stimulated signaling proteins involved in glucose transport, muscle fiber type, and mitochondrial biogenesis is ongoing. Further research is needed because full elucidation of exercise-mediated signaling pathways would represent a significant step toward the development of new pharmacological targets for the treatment of metabolic diseases such as type 2 diabetes. |
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Authors:
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Katja S C Röckl; Carol A Witczak; Laurie J Goodyear |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: IUBMB life Volume: 60 ISSN: 1521-6543 ISO Abbreviation: IUBMB Life Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-04-01 Completed Date: 2008-05-22 Revised Date: 2011-08-01 |
Medline Journal Info:
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Nlm Unique ID: 100888706 Medline TA: IUBMB Life Country: England |
Other Details:
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Languages: eng Pagination: 145-53 Citation Subset: IM |
Affiliation:
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Research Division, Joslin Diabetes Center and Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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AMP-Activated Protein Kinases Adaptation, Physiological* Calcineurin / metabolism Calcium-Calmodulin-Dependent Protein Kinases / metabolism Cyclic AMP-Dependent Protein Kinases / metabolism Exercise* GTPase-Activating Proteins / metabolism Glucose / metabolism Heat-Shock Proteins Humans Multienzyme Complexes / metabolism Muscle, Skeletal / cytology, physiology* Protein Kinase C / metabolism Protein-Serine-Threonine Kinases / metabolism Signal Transduction / physiology* Transcription Factors p38 Mitogen-Activated Protein Kinases / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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DK36836/DK/NIDDK NIH HHS; F32 AR051663-02/AR/NIAMS NIH HHS; F32AR051663/AR/NIAMS NIH HHS; P30 DK036836-21/DK/NIDDK NIH HHS; R01 AR045670-10/AR/NIAMS NIH HHS; R01 DK068626-04/DK/NIDDK NIH HHS; R01AR45670/AR/NIAMS NIH HHS; R01DK068626/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/GTPase-Activating Proteins; 0/Heat-Shock Proteins; 0/Multienzyme Complexes; 0/PPARGC1A protein, human; 0/TBC1D4 protein, human; 0/Transcription Factors; 50-99-7/Glucose; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.11/Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 3.1.3.16/Calcineurin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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