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Mediation of testosterone action in muscle by growth hormone / IGF‐1 signaling
Author(s) -
Morris Carl A,
Morris Linda,
Jiang Lan,
LeBrasseur Nathan,
Jasuja Ravi,
Flanagan John,
Bhasin Shalender
Publication year - 2007
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.21.6.a947
Subject(s) - testosterone (patch) , endocrinology , medicine , mediation , action (physics) , growth hormone , hormone , political science , physics , quantum mechanics , law
Testosterone (T) is considered a potent anabolic agent that increases muscle mass and strength in humans. Similarly, growth hormone (GH) and insulin‐like growth factor‐1 (IGF‐1) have been identified as critical mediators of muscle mass and strength. GH and T exhibit apparent synergism in various populations such as elderly men and prepubertal boys. It is thought that testosterone functions via an androgen receptor‐mediated pathway and it’s downstream signaling (e.g. Wnt /β‐catenin). However, T may interact directly with the GH/IGF‐I axis to stimulate growth and/or reduce muscle wasting independently of any AR‐mediated response. T was found to stimulate GH secretion and production of liver IGF‐1, and also to increase IGF‐1 mRNA and protein levels in skeletal muscle. Thus it appears that testosterone confers part of its effects via the GH/IGF‐I signaling pathway. To test this, we administered either oil or testosterone enanthate (TE) to rats that had been castrated (C), hypophysectomized (H), or both (CH). The body and muscle were weighed and serum and tissue samples stored. In the C, H, and CH groups, the androgen‐responsive levator ani muscle exhibited a dose‐dependent increase in mass with TE administration. Further, IGF‐1Ea and IGF‐1Eb (MGF) mRNA expression increased with TE in all three groups (C, H, and CH). These results suggest that the anabolic effects of TE are independent of GH signaling, but are possibly associated with local IGF‐1 signaling.

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