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β‐Adrenergic Stimulation improves mitochondrial function and markers of biogenesis and dynamics in human primary myotubes
Author(s) -
Frisard Madlyn Irene,
Werner Tim,
Hulver Matthew W,
Davy Kevin P
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1051.4
Subject(s) - ampk , myogenesis , mitochondrial biogenesis , endocrinology , medicine , protein kinase a , phosphorylation , stimulation , chemistry , mitochondrion , biology , myocyte , microbiology and biotechnology
The β‐adrenergic signaling pathway has long been studied for its potential to prevent or treat muscle wasting associated with muscle disease. The purpose of this study was to identify the role of β‐adrenergic stimulation on mitochondrial function in human primary myotubes and whether it is dependent on 5′ adenosine monophosphate‐activated protein kinase (AMPK). Myotubes were treated with 10μM of isoproterenol with or without the AMPK inhibitor compound C for 2 hours and oxygen consumption, mRNA and AMPK phosphorylation were assessed. β‐adrenergic stimulation resulted in an increase in AMPK phosphorylation, which was blocked by compound C. Isoproterenol also resulted in a significant increase (+125%, p<0.05) in maximal oxygen consumption that coincided with an up regulation of peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (17‐fold), optic atrophy protein 1 (1.7‐fold), and dynamin related protein 1 (1.5‐fold) mRNA (all, p<0.05). These effects were partially attenuated in the presence of compound C. In conclusion, the current study suggests that β‐adrenergic stimulation improves mitochondrial function and content in human myotubes, which is partially dependent on AMPK phosphorylation.