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Altered content of AMP-activated protein kinase isoforms in skeletal muscle from spinal cord injured subjects
Sunnaas Rehabilitation Hospital, Nesoddtangen, Norway & University of Oslo, Oslo, Norway.
Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.ORCID iD: 0000-0003-4235-0634
Sunnaas Rehabilitation Hospital, Nesoddtangen, Norway.
Departments of Physiology and Pharmacology, Section for Integrative Physiology, Karolinska Institutet, Stockholm, Sweden.
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2013 (English)In: American Journal of Physiology. Endocrinology and Metabolism, ISSN 0193-1849, E-ISSN 1522-1555, Vol. 305, no 9, E1071-E1080 p.Article in journal (Refereed) Published
Abstract [en]

AMP-activated protein kinase (AMPK) is a pivotal regulator of energy homeostasis. Although downstream targets of AMPK are widely characterized, the physiological factors governing isoform expression of this protein kinase are largely unknown. Nerve/contractile activity has a major impact on the metabolic phenotype of skeletal muscle, therefore likely to influence AMPK isoform expression. Spinal cord injury represents an extreme form of physical inactivity, with concomitant changes in skeletal muscle metabolism. We assessed the influence of longstanding and recent spinal cord injury on protein abundance of AMPK isoforms in human skeletal muscle. We also determined muscle fiber type as a marker of glycolytic or oxidative metabolism. In subjects with longstanding complete injury, protein abundance of the AMPKγ3 subunit, as well as myosin heavy chain (MHC) IIa and IIx, were increased, whereas abundance of the AMPKγ1 subunit and MHC I were decreased. Similarly, abundance of AMPKγ3 and MHC IIa proteins were increased, whereas AMPKα2, -β1, and -γ1 subunits and MHC I abundance was decreased during the first year following injury, reflecting a more glycolytic phenotype of the skeletal muscle. However, in incomplete cervical lesions, partial recovery of muscle function attenuated the changes in the isoform profile of AMPK and MHC. Furthermore, exercise training (electrically stimulated leg cycling) partly normalized mRNA expression of AMPK isoforms. Thus, physical activity affects the relative expression of AMPK isoforms. In conclusion, skeletal muscle abundance of AMPK isoforms is related to physical activity and/or muscle fiber type. Thus, physical/neuromuscular activity is an important determinant of isoform abundance of AMPK and MCH. This further underscores the need for physical activity as part of a treatment regimen after spinal cord injury to maintain skeletal muscle metabolism. © 2013 the American Physiological Society.

Place, publisher, year, edition, pages
Bethesda, MD: American Physiological Society , 2013. Vol. 305, no 9, E1071-E1080 p.
Keyword [en]
physical inactivity, muscle, metabolism, spinal cord injury
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:hh:diva-26616DOI: 10.1152/ajpendo.00132.2013ISI: 000326578600003PubMedID: 24022865Scopus ID: 2-s2.0-84887013288OAI: oai:DiVA.org:hh-26616DiVA: diva2:750416
Available from: 2014-09-29 Created: 2014-09-29 Last updated: 2015-09-29Bibliographically approved

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