Abstract
The addition of recombinant human interleukin-6 (rIL-6) to either soleus or extensor digitorum longus (EDL) muscle preparations did not affect the rate of protein breakdown as measured by the rate of tyrosine released to the medium. In addition, the presence of the cytokine did not influence either the rate of protein synthesis or that of α-(methyl)-aminoisobutyric acid (MeAIB) uptake by the muscle preparations. It is concluded that IL-6 is not the mediator in activating muscle protein turnover during sepsis in the rat.
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