Effect of β-agonists on expression of calpain and calpastatin activity in skeletal muscle

• Published in: Biochimie Vol. 74; no. 3; pp. 267 - 273
• Main Authors: Bardsley, R.G., Allock, S.M.J., Allcock, S.M.J., Dumelow, N.W., Higgins, J.A., Lasslett, Y.V., Lockley, A.K., Parr, T., Buttery, P.J.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Paris Elsevier Masson SAS 01.03.1992; Elsevier
• Subjects: Adrenergic beta-Agonists - pharmacology; Analytical, structural and metabolic biochemistry; Animals; Biological and medical sciences; Calcium-Binding Proteins - genetics; calpain; Calpain - genetics; calpastatin; Cattle; Chickens; Enzymes and enzyme inhibitors; Ethanolamines - pharmacology; Female; Fundamental and applied biological sciences. Psychology; Gene Expression - drug effects; growth; Hydrolases; Male; Muscles - drug effects; Muscles - enzymology; Rats; Rats, Inbred Strains; RNA, Messenger - metabolism; Sheep; skeletal muscle; β-agonists; β-agonists; calpain; calpastatin; growth; skeletal muscle
• ISSN: 0300-9084; 1638-6183
• DOI: 10.1016/0300-9084(92)90125-X

Administration of β-adrenergic agonists to domestic species can lead to skeletal muscle hypertrophy, probably by reducing the rate of myofibrillar protein breakdown. Myofibrillar breakdown is associated with the calcium-dependent proteinase system (calpains I, II and calpastatin) whose activity also changes during β-agonist treatment. A number of growth trials using the agonists cimaterol and clenbuterol with cattle, sheep, chicken and rat are reported which suggest a general mechanism whereby β-agonists reduce calpain I activity, but increase calpain II and calpastatin activity in skeletal muscle. Parallel changes in specific mRNAs indicate that changes in gene expression or stabilisation of mRNA could in part explain the changes in activity.