Cited by 80Growth Hormone and Insulin-like Growth FactorsMuscle metabolism and nutritionMuscle Physiology and Disorders

Enhancement of muscle mitochondrial function by growth hormone

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Short, Kevin R., Moller, Niels, Bigelow, Maureen L., Coenen-Schimke, Jill, Nair, K. Sreekumaran·2008·The Journal of Clinical Endocrinology & Metabolism

Abstract

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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Crossref · 10.1210/jc.2007-1814

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  • Acute GH administration in healthy young humans, which increases IGF-1, promotes an increase in mitochondrial oxidative capacity and abundance of various mitochondrial genes in skeletal muscle.

    “However, acute GH administration in healthy young humans, which increases IGF-1, promotes an increase in mitochondrial oxidative capacity and the abundance of various mitochondrial genes in skeletal muscle.137”

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Authors
Short, K. R., Moller, N., Bigelow, M. L., Coenen-Schimke, J., & Nair, K. S.
Affiliations
  • Mayo Clinic (US)
  • Endocrinology Research Unit, Mayo Clinic School of Medicine, Rochester, Minnesota 55905
Corresponding author
Nair, K. Sreekumaran
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
2008-02-01
Volume
93
Issue
2
Pages
597-604
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
OpenAlex
W2096421773
Cited by
80
References
57
Citations by year
2026: 2 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 7 · 2018: 6 · 2017: 4 · 2016: 5 · 2015: 6 · 2014: 5 · 2013: 6 · 2012: 8
FWCI
3.90
Type
journal article
Language
en
Open access
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Mayo Clinic
  • Mayo Foundation for Medical Education and Research
  • Deutsches Krebsforschungszentrum
  • National Institutes of Health (RR-00585)
  • National Institute of Diabetes and Digestive and Kidney Diseases (T32-DK-07352, R01DK41973, R01DK041973, T32DK007352)
  • National Center for Research Resources (M01-RR00 585, M01RR000585)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
Keywords
growth hormone, skeletal muscle, mitochondrial function, oxidative capacity, citrate synthase, insulin-like growth factor I, mitochondrial gene expression, cytochrome c oxidase, TFAM, glucose transporter 4, fat oxidation, leucine oxidation, protein synthesis, fuel selection
MeSH terms
Adenosine Triphosphate, Adult, Biopsy, Citrate (si)-Synthase, Female, Humans, Insulin-Like Growth Factor I, Male, Mitochondria, Muscle, Muscle Proteins, RNA, Messenger, Muscle, Skeletal, Cross-Over Studies, Human Growth Hormone, Reverse Transcriptase Polymerase Chain Reaction, Mitochondrial Proteins

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