| Enhancement of muscle mitochondrial function by growth hormone. | |
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MedLine Citation:
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PMID: 18000087 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Although GH promotes growth and protein anabolism, which are ATP-dependent processes, the GH effect on mitochondrial regulation remains to be determined. OBJECTIVE: Our objective was to determine the acute effect of GH on mitochondrial oxidative capacity in skeletal muscle of healthy subjects. DESIGN AND SETTING: The study was a randomized crossover design at an academic medical center. PARTICIPANTS: Nine healthy men and women completed the study. INTERVENTION: GH (150 microg/h) or saline was infused for 14 h on separate days, and muscle biopsies were obtained. MAIN OUTCOME MEASURES: Outcome measures included mitochondrial function, gene expression, and protein metabolism. RESULTS: The 4-fold increase in plasma GH caused elevations in plasma IGF-I, insulin, glucose, and free fatty acids and a shift in fuel selection, with less carbohydrate (-69%) and leucine (-43%) oxidation and 29% more fat oxidation. Muscle mitochondrial ATP production rate and citrate synthase activity were increased 16-35% in response to GH. GH also resulted in higher abundance of muscle mRNAs encoding IGF-I, mitochondrial proteins from the nuclear (cytochrome c oxidase subunit 4) and mitochondrial (cytochrome c oxidase subunit 3) genomes, the nuclear-derived mitochondrial transcription factor A, and glucose transporter 4. Although GH increased whole-body protein synthesis (nonoxidative disposal of leucine), no effect on synthesis rate of muscle mitochondrial proteins was observed. CONCLUSIONS: These results demonstrate that acute GH action promotes an increase in mitochondrial oxidative capacity and abundance of several mitochondrial genes. These events may occur through direct or indirect effects of GH on intracellular signaling pathways but do not appear to involve a change in mitochondrial protein synthesis rate. |
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Authors:
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Kevin R Short; Niels Moller; Maureen L Bigelow; Jill Coenen-Schimke; K Sreekumaran Nair |
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Publication Detail:
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Type: Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2007-11-13 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 93 ISSN: 0021-972X ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2008 Feb |
Date Detail:
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Created Date: 2008-02-08 Completed Date: 2008-04-10 Revised Date: 2013-03-05 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 597-604 Citation Subset: AIM; IM |
Affiliation:
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Endocrinology Research Unit, Mayo Clinic School of Medicine, 5-194 Joseph, 200 First Street SW, Rochester, Minnesota 55905, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism Adult Biopsy Citrate (si)-Synthase / metabolism Cross-Over Studies Female Human Growth Hormone / pharmacology* Humans Insulin-Like Growth Factor I / biosynthesis, genetics Male Mitochondria, Muscle / drug effects*, enzymology, metabolism, physiology Mitochondrial Proteins / biosynthesis, genetics Muscle Proteins / metabolism Muscle, Skeletal / drug effects*, physiology RNA, Messenger / biosynthesis, genetics Reverse Transcriptase Polymerase Chain Reaction |
| Grant Support | |
ID/Acronym/Agency:
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M01-RR00585/RR/NCRR NIH HHS; R01-DK41973/DK/NIDDK NIH HHS; T32-DK07352/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Mitochondrial Proteins; 0/Muscle Proteins; 0/RNA, Messenger; 12629-01-5/Human Growth Hormone; 56-65-5/Adenosine Triphosphate; 67763-96-6/Insulin-Like Growth Factor I; EC 2.3.3.1/Citrate (si)-Synthase |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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