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R. H. McCusker
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D. R. Campion
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ABSTRACT

Tumours secreting GH (GH1) or GH plus prolactin (GH3) were induced in young (1-week-old) and mature (17-week-old) female Wistar–Furth rats. Young animals were killed at 11 weeks and mature rats at 30 weeks of age. Induction of tumours increased serum GH concentrations and body and soleus muscle weights when compared with those of control rats. The soleus and extensor digitorum longus (EDL) muscles were examined in transverse section by electron microscopy. The percentages of myofibres with myonuclei and with satellite cell nuclei present in both the soleus and EDL muscles were generally greater in young rats with tumours than in young control rats. The percentage of myofibres in the EDL muscle with myonuclei present was higher in mature rats with GH1 tumours compared with age-matched controls. The presence of tumours did not affect the number of fibres in the soleus muscle of either young or mature rats. It was concluded that increased GH concentrations increased muscle weight by increasing the DNA content of myofibres and by myofibre hypertrophy. The rate of proliferation of satellite cells apparently exceeded the rate of incorporation of daughter nuclei into the fibres of the young tumourbearing rats when compared with that of young controls. Thus, the factors regulating satellite cell proliferation and nuclear incorporation into the myofibre do not appear to be directly coupled.

J. Endocr. (1986) 111, 279–285

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.0.1110279
Volume/Issue:
Volume 111: Issue 2
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Alexander Hennebry AgResearch Ltd, Hamilton, New Zealand

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Jenny Oldham AgResearch Ltd, Hamilton, New Zealand

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Tea Shavlakadze School of Anatomy, Physiology & Human Biology, The University of Western Australia, Crawley, Western Australia, Australia

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Miranda D Grounds School of Anatomy, Physiology & Human Biology, The University of Western Australia, Crawley, Western Australia, Australia

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Philip Sheard Department of Physiology, University of Otago, Dunedin, New Zealand

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Marta L Fiorotto USDA/ARS Children’s Nutrition Research Center, Baylor College of Medicine, Houston, Texas, USA

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Shelley Falconer AgResearch Ltd, Hamilton, New Zealand

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Heather K Smith Department of Exercise Sciences, University of Auckland, Auckland, New Zealand

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Carole Berry AgResearch Ltd, Hamilton, New Zealand

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Ferenc Jeanplong AgResearch Ltd, Hamilton, New Zealand

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Jeremy Bracegirdle AgResearch Ltd, Hamilton, New Zealand

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Kenneth Matthews AgResearch Ltd, Hamilton, New Zealand

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Gina Nicholas AgResearch Ltd, Hamilton, New Zealand

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Mônica Senna-Salerno AgResearch Ltd, Hamilton, New Zealand

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Trevor Watson AgResearch Ltd, Hamilton, New Zealand

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Christopher D McMahon AgResearch Ltd, Hamilton, New Zealand

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myofibres ( Lee & McPherron 2001 ). However, when myostatin activity is blocked, hypertrophy still requires the presence of IGF1 receptors ( Kalista et al. 2012 , Winbanks et al. 2012 ). Therefore, it appears that IGF1 is critical for enabling the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0032
Volume/Issue:
Volume 234: Issue 2
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Ryan Paul University of Auckland Waikato Clinical School, Hamilton, New Zealand

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Kim Whiteman ManukaMed LP, Hamilton, New Zealand

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Shelley J Falconer AgResearch Ltd, Hamilton, New Zealand

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Jenny M Oldham AgResearch Ltd, Hamilton, New Zealand

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Ferenc Jeanplong AgResearch Ltd, Hamilton, New Zealand

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Kenneth G Matthews AgResearch Ltd, Hamilton, New Zealand

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Heather K Smith Department of Exercise Sciences, University of Auckland, Auckland Mail Centre, Auckland, New Zealand

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Mark Thomas ManukaMed LP, Hamilton, New Zealand

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Trevor Watson AgResearch Ltd, Hamilton, New Zealand

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Christopher D McMahon ManukaMed LP, Hamilton, New Zealand
AgResearch Ltd, Hamilton, New Zealand

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-natal life ( Beilharz et al. 1992 ). This is consistent with IGF1 acting to increase hypertrophy of muscle fibres rather than regulating hyperplasia. In contrast, reduced abundance, or absence of myostatin increases hyperplasia of myofibres ( Hennebry et

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-20-0485
Volume/Issue:
Volume 248: Issue 2
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Eileen I Chang Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Paul J Rozance Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Stephanie R Wesolowski Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Leanna M Nguyen Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Steven C Shaw Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Robert A Sclafani Department of Biochemistry and Molecular Genetics, University of Colorado School of Medicine, Aurora, Colorado, USA

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Kristen K Bjorkman Department of Molecular, Cellular and Developmental Biology and BioFrontiers Institute, University of Colorado Boulder, Boulder, Colorado, USA

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Angela K Peter Department of Molecular, Cellular and Developmental Biology and BioFrontiers Institute, University of Colorado Boulder, Boulder, Colorado, USA

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William W Hay Jr Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Laura D Brown Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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proliferation, differentiation, and fusion of satellite cells is an essential regulator of muscle fiber growth by hypertrophy ( White et al. 2010 , Blaauw & Reggiani 2014 , Egner et al. 2016 , Snijders et al. 2016 , Dungan et al. 2019 ); thus

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0273
Volume/Issue:
Volume 244: Issue 2
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A M Solomon Department of Endocrinology, Royal Free Hospital and Medical School, Pond Street, London NW3 2PF, UK

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P M G Bouloux Department of Endocrinology, Royal Free Hospital and Medical School, Pond Street, London NW3 2PF, UK

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Metabolism 88 2784 –2793. Armand AS , Lecolle S, Launay T, Pariset C, Fiore F, Della GB, Birnbaum D, Chanoine C & Charbonnier F 2004 IGF-II is up-regulated and myofibres are hypertrophied in regenerating soleus of mice

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Review Article
DOI:
https://doi.org/10.1677/joe.1.06837
Volume/Issue:
Volume 191: Issue 2
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Manon M Roustit
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Joan M Vaughan Department of Comparative Biomedical Sciences, Laboratory of Neuronal Structure and Function, Queen's Medical Research Institute, Royal Veterinary College, University of London, Royal College Street, London NW1 0TU, UK

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Pauline M Jamieson Department of Comparative Biomedical Sciences, Laboratory of Neuronal Structure and Function, Queen's Medical Research Institute, Royal Veterinary College, University of London, Royal College Street, London NW1 0TU, UK

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Mark E Cleasby
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treatments available. However, recent work has demonstrated that generalised overexpression of urocortin 3 (UCN3) in mice results in both hypertrophy and increased glucose disposal into muscle ( Jamieson et al . 2011 ), making this an interesting candidate

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Research Article
DOI:
https://doi.org/10.1530/JOE-14-0181
Volume/Issue:
Volume 223: Issue 2
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Laura D Brown Department of Pediatrics (Neonatology), Perinatal Research Center, University of Colorado School of Medicine, Anschutz Medical Campus F441, 13243 East 23rd Avenue, Aurora, Colorado 80045, USA

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results in the withdrawal of myoblasts from the cell cycle and subsequent fusion into myotubes. Myotube maturation and hypertrophy are stimulated by growth factors, amino acids, and stretch/load activity ( Molkentin & Olson 1996 , Yang & Makita 1996

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-13-0567
Volume/Issue:
Volume 221: Issue 2
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M Granado Department of Physiology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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A I Martín Department of Physiology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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T Priego Department of Physiology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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A López-Calderón Department of Physiology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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M A Villanúa Department of Physiology, Faculty of Medicine, Complutense University, 28040 Madrid, Spain

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mass by enhancing myofibre hypertrophy and stimulating myogenesis ( Musaro et al. 2001 ). However, it has been reported ( Foulstone et al. 2001 ) that the effects of IGF-I on muscle may depend on the cytokine environment in such a way that in the

Article Type:
Research Article
DOI:
https://doi.org/10.1677/joe.1.06931
Volume/Issue:
Volume 191: Issue 1
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Sonnet S Jonker Center for Developmental Health, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon, USA

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Daniel Kamna Center for Developmental Health, Knight Cardiovascular Institute, Oregon Health & Science University, Portland, Oregon, USA

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Dan LoTurco Department of Pediatrics, Perinatal Research Center, Anschutz Medical Campus, University of Colorado, Aurora, Colorado, USA

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Jenai Kailey Department of Pediatrics, Perinatal Research Center, Anschutz Medical Campus, University of Colorado, Aurora, Colorado, USA

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Laura D Brown Department of Pediatrics, Perinatal Research Center, Anschutz Medical Campus, University of Colorado, Aurora, Colorado, USA

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repression in the heart. How cortisol interacts with low levels of IGF1 to suppress growth or induce apoptosis in IUGR skeletal and cardiac muscle remains to be determined. Norepinephrine is a non-selective adrenergic agonist linked to hypertrophy in adult

Article Type:
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DOI:
https://doi.org/10.1530/JOE-18-0382
Volume/Issue:
Volume 239: Issue 2
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Susan M Soto Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Amy C Blake Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Stephanie R Wesolowski Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Paul J Rozance Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Kristen B Barthel Department of Molecular, Cellular, and Developmental Biology, University of Colorado Boulder, BioFrontiers Institute, Boulder, Colorado, USA

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Bifeng Gao Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA

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Byron Hetrick Department of Human Physiology, University of Oregon, Eugene, Oregon, USA

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Carrie E McCurdy Department of Human Physiology, University of Oregon, Eugene, Oregon, USA

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Natalia G Garza Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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William W Hay Jr Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Leslie A Leinwand Department of Molecular, Cellular, and Developmental Biology, University of Colorado Boulder, BioFrontiers Institute, Boulder, Colorado, USA

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Jacob E Friedman Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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Laura D Brown Department of Pediatrics, University of Colorado School of Medicine, Perinatal Research Center, Aurora, Colorado, USA

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postnatal muscle growth occurs primarily by hypertrophy ( Rowe & Goldspink 1969 , Wigmore & Stickland 1983 , Fahey et al . 2005 b ). Myogenesis is regulated in part by the fetal growth factors, particularly insulin and insulin-like growth factors (IGFs

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0123
Volume/Issue:
Volume 232: Issue 3
Free access