Lack of effect of anabolic steroids on specific mRNAs of skeletal muscle undergoing compensatory hypertrophy

• Published in: Molecular and cellular endocrinology Vol. 51; no. 1; pp. 19 - 24
• Main Authors: Boissonneault, G., Gagnon, J., Ho-Kim, M.A., Tremblay, R.R.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.05.1987; Elsevier
• Subjects: Anabolic Agents - pharmacology; Androgen; Animals; Biological and medical sciences; Fluoxymesterone - pharmacology; Gene Expression Regulation - drug effects; Hormones. Endocrine system; Hypertrophy; Male; Medical sciences; Muscle Proteins - metabolism; Muscles - drug effects; Muscles - pathology; Myosins - genetics; Nandrolone - pharmacology; Orchiectomy; Pharmacology. Drug treatments; Protein synthesis; Rats; Receptors, Androgen - metabolism; RNA, Messenger - genetics; Skeletal muscle; Stanozolol - pharmacology; Testosterone - pharmacology; Tropomyosin - genetics; Androgen; Protein synthesis; Skeletal muscle; Hypertrophy; Steroid; Rat; Rodentia; Striated muscle; Vertebrata; Compensatory hypertrophy; Mammalia; Messenger RNA; Animal; Anabolic agent; Biological receptor
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/0303-7207(87)90114-6

Compensatory hypertrophy of the fast-twitch plantaris muscle (HP) was induced in male rats to determine whether the resulting translational activity of isolated polyribosomes could be modified in this process and by the androgen status. HP induced a significant increase in free androgen binding sites and a typical protein synthesis pattern characterized by a slow myosin light chain isozyme (LC-1S), an increase in fast isozymes (LC-1F,2F) and of β-tropomyosin/α-tropomyosin ratio. The variations in receptor occupancy following castration and treatments with four anabolic steroids (AS) did not result in modification of the template activity of major HP mRNAs. These data suggest that the slight increase of steroid receptors found in HP remains unsufficient to trigger an androgenic response in skeletal muscle.