Countereffects of compensatory overload and glucocorticoids in skeletal muscle: Androgen and glucocorticoid cytosol receptor binding

T. T. Kurowski, R. T. Chatterton, R. C. Hickson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Male hypophysectomized rats were divided into a control group and a group that was subjected to compensatory overload of plantaris muscles for 7 days following surgical removal of synergistic musculature. These groups received daily subcutaneous injections of either cortisone acetate (CA) (100 mg/kg b.wt) or the vehicle for 7 days starting at the time the overload was initiated. Plantaris muscle weights were atrophied by 25% in CA-treated controls, were hypertrophied by 45% in the vehicle-treated overloaded group, and remained similar to vehicle-treated controls in the group receiving both treatments. Scatchard analyses of specific binding of [3H]methyltrienolone (R1881), a synthetic androgen that binds to androgen receptors, were non-linear in plantaris muscle cytosols of vehicle-treated control and overloaded groups and were resolved by a two-component binding model. The lower affinity component, which was attributed to binding of methyltrienolone to a glucocorticoid receptor, disappeared in glucocorticoid-treated rats as evidenced by linear Scatchard plots. Receptor concentrations of the androgenic component of [3H]methyltrienolone binding were unchanged by CA treatment and were significantly increased only in the vehicle-treated overloaded group. [3H]Dexamethasone cytosol binding was increased nearly 2-fold in plantaris muscles of vehicle-treated overloaded animals (64 ± 3 fmol/mg protein) as compared to those in vehicle-treated controls (32 ± 2 fmol/mg protein), but was decreased to 2 and 4 fmol/mg protein in the CA-treated controls and CA-treated overloaded groups respectively. These results show that overload and glucocorticoids have opposing actions skeletal muscle, but the overload in the presence of glucocorticoids did not stimulate an increase in androgen cytosol receptor binding.

Original languageEnglish (US)
Pages (from-to)137-145
Number of pages9
JournalJournal of Steroid Biochemistry
Issue number2
StatePublished - Aug 1984


  • 17β-estradiol, 1, 3, 5, (10)-estratriene-3, 17β-diol
  • 5α-dihydrotestosterone, 17β-hydroxy-5α-androstan-3-one
  • Cortisol (F), 11β, 17, 21-trihydroxy-4-pregnene-3, 20-dione
  • Dianabol (methandrostenolone), 17β-hydroxy-17α-methyladrosta-1, 4-diene-3-one
  • Methyltrienolone (R1881), 17β-hydroxy-17α-methyl-estra-4, 9, 11-trien-3-one
  • corticosterone (B), 11β, 21-dihydroxy-4-pregnene-3, 20-dione
  • cortisone, 17α, 21-dihydroxy-4-pregnene-3, 11, 20-trione
  • dexamethasone, 9α-fluoro-11β, 17, 21-trihydroxy-16α-methyl-pregna-1, 4-diene-3, 20-dione
  • progesterone, 4-pregnene-3, 20-dione
  • testosterone, 17β-hydroxy-4-androsten-3-one
  • triamicinolone acetonide, 9α-fluoro-11β, 16, 17, 21-tetrahydroxy-pregna-1, 4-diene-3, 20-dione cyclic 16, 17-acetal

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology


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