Effect of circulating growth hormone on muscle IGF-I protein concentration in female mice with growth hormone receptor gene disruption |
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Authors: | William J. Kraemer Jakob L. Vingren Mark D. Schuenke John J. Kopchick Jeff S. Volek Maren S. Fragala Keijo Häkkinen Gwendolyn A. Thomas Robert S. Staron |
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Affiliation: | 1. Human Performance Laboratory, Department of Kinesiology, University of Connecticut, 2095 Hillside Road Unit 1110, Gampel Pavilion, Storrs, CT 06269-1110, USA;2. Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT 06269, USA;3. Department of Kinesiology, Health Promotion and Recreation, University of North Texas, Denton, TX 76203, USA;4. Department of Anatomy, College of Osteopathic Medicine, University of New England, Biddeford ME 04005, USA;5. Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, OH 45701, USA;6. Department of Biology of Physical Activity and Neuromuscular Research Center, University of Jyväskylä, Jyväskylä, Finland |
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Abstract: | Growth hormone (GH) is a potent secretague for circulating insulin-like growth factor-I (IGF-I). The purpose of this study was to examine the effect of circulating GH on muscle IGF-I protein expression using GH transgenic animal models. Three different models were used: mice that overexpress bovine GH (bGH; n = 10), mice without a functional GH receptor (GHR-/-; n = 10), and wildtype mice (n = 10). All mice were 16-week old females and each group differed in their basic phenotypic characteristics. Immediately after euthanization the triceps surae muscle group (soleus, plantaris, and gastrocnemius muscles) was removed. IGF-I was extracted from the muscle with an acid–ethanol solution (12.5% 2N hydrochloric acid and 87.5% ethanol, pH 1.5) followed by neutralization with Tris-base and subsequently quantified using a radioimmunoassay. Analysis revealed that bGH mice had significantly greater muscle IGF-I protein expression compared to GHR-/- and wildtype mice. No difference in IGF-I protein concentration was found between GHR-/- and wildtype animals. This study found that overexpression of GH leading to high circulating GH concentrations increase muscle IGF-I protein expression. However, the absence of a functional GHR did not affect muscle IGF-I protein expression compared to wildtype despite high circulating levels of GH and low circulating levels of IGF-I. In conclusion, it appears that at rest high circulating levels of GH augment muscle IGF-I protein expression only in the presence of an intact GHR but that the absence of a functional GH receptor does not affect basal levels of muscle IGF-I protein in female mice. |
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