More Lean, Less Fat With Clenbuterol

There is too much fat on beef carcasses today. Research in beef cattle production is directed towards solving this problem by maximizing partitioning of dietary nutrients to lean muscle growth and minimizing deposition of carcass fat. Partitioning agents called β - adrenergic agonists are able to cause this type of nutrient partitioning. Earlier work showed two of these compounds, clenbuterol and cimaterol, can be fed and are effective in many species including pigs, sheep, and cattle. At levels that did not depress gain, clenbuterol feeding increased protein content of the 9th to 11th rib section by 13% and decreased fat content by 20% in cattle. Even more dramatic carcass changes were observed in cattle in response to cimaterol. Of interest are the underlying metabolic changes and controls that must be altered to bring about the carcass changes previously cited. To date, the mechanisms responsible for altering nutrient partitioning in response to β-adrenergic agonists are not well defined. The objectives of our study were to compare the initial and adapted effects of clenbuterol on blood flow, heart rate, and metabolism in the hindquarters of growing steers

MEK5 and ERK5 are mediators of the pro-myogenic actions of IGF-2

During the differentiation of muscle satellite cells, committed myoblasts respond to specific signalling cues by exiting the cell cycle, migrating, aligning, expressing muscle-specific genes and finally fusing to form multinucleated myotubes. The predominant foetal growth factor, IGF-2, initiates important signals in myogenesis. The aim of this study was to investigate whether ERK5 and its upstream MKK activator, MEK5, were important in the pro-myogenic actions of IGF-2. ERK5 protein levels, specific phosphorylation and kinase activity increased in differentiating C2 myoblasts. ERK5-GFP translocated from the cytoplasm to the nucleus after activation by upstream MEK5, whereas phospho-acceptor site mutated (dominant-negative) ERK5AEF-GFP remained cytoplasmic. Exogenous IGF-2 increased MHC levels, myogenic E box promoter-reporter activity, ERK5 phosphorylation and kinase activity, and rapidly induced nuclear localisation of ERK5. Transfection with antisense Igf2 decreased markers of myogenesis, and reduced ERK5 phosphorylation, kinase and transactivation activity. These negative effects of antisense Igf2 were rescued by constitutively active MEK5, whereas transfection of myoblasts with dominant-negative MEK5 blocked the pro-myogenic action of IGF-2. Our findings suggest that the MEK5-ERK5 pathway is a novel key mediator of IGF-2 action in myoblast differentiation