Anabolic effects of feeding beta2-adrenergic agonists on rainbow trout muscle proteases and proteins.
beta2-Adrenergic agonists (BAAs) act as repartitioning agents in domestic animals by redistributing nutrients away from adipose tissue and towards muscle accretion. The mechanism involves altering the rates of protein degradation and synthesis. The aim of this study was to test the effects of chronic feeding of the BAAs clenbuterol (CLEN) and ractopamine (RACT) on rainbow trout (RBT) muscle. Specifically, we examined the activities and mRNA levels of genes in the major proteolytic pathways including calpains, the multi-catalytic proteasome and cathepsins, and the mRNA levels of genes encoding the myofibrillar proteins, fast-twitch and slow-twitch myosin heavy chains (f-MHC and s-MHC, respectively), and the cytoskeletal protein, beta-actin. RACT feeding significantly increased mRNA transcripts of the calpain catalytic subunit (Capn1), the regulatory subunit (cpns), and the calpastatin large isoform (CAST-L), without affecting the calpain enzyme activity. CLEN feeding significantly increased mRNA levels of the proteasome alpha subunit without a corresponding change in 20S enzyme activity. RACT significantly decreased cathepsin D activity without affecting mRNA levels suggesting that the action of RACT may be at the post-transcriptional level. In addition, both CLEN and RACT significantly increased mRNA transcripts of f-MHC and beta-actin genes suggesting an anabolic role of BAAs on myofibrillar and cytoskeletal proteins. Neither CLEN nor RACT altered mRNA expression of the s-MHC gene indicating no transformation of muscle fiber-types. This study supports a role for BAAs in inducing RBT muscle accretion by altering both protein synthesis and degradation.
Salem
Mohamed
M
Division of Animal and Veterinary Sciences, West Virginia University, Morgantown, WV 26506-6108, USA.
Levesque
Haude
H
Moon
Thomas W
TW
Rexroad
Caird E
CE
Yao
Jianbo
J
D051697:Activating Transcription Factor 1 / Q000378:metabolism; D000262:Adenylyl Cyclases / Q000378:metabolism; D000318:Adrenergic beta-Agonists / Q000009:adverse effects*; D000595:Amino Acid Sequence; D000821:Animal Feed / Q000009:adverse effects; D000818:Animals; D002154:Calpain / Q000378:metabolism; D002403:Cathepsins / Q000378:metabolism; D002976:Clenbuterol / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D018076:DNA, Complementary; D008969:Molecular Sequence Data; D009124:Muscle Proteins / Q000378:metabolism*; D009132:Muscles / Q000187:drug effects* / Q000201:enzymology; D017686:Oncorhynchus mykiss / Q000378:metabolism*; D010447:Peptide Hydrolases / Q000378:metabolism*; D010627:Phenethylamines / Q000494:pharmacology; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism; D017386:Sequence Homology, Amino Acid
D051697:Activating Transcription Factor 1; D000318:Adrenergic beta-Agonists; D018076:DNA, Complementary; D009124:Muscle Proteins; D010627:Phenethylamines; D018343:Receptors, Adrenergic, beta-2; C060897:ractopamine; D000242:Cyclic AMP; D002403:Cathepsins; D010447:Peptide Hydrolases; D002154:Calpain; D046988:Proteasome Endopeptidase Complex; D000262:Adenylyl Cyclases; D002976:Clenbuterol