Abstract
SummaryCreatine entry into isolated extensor digitorum longus muscles of normal and of dystrophic mice was studied with the aid of creatine-14C as a tracer. The creatine entry process in mouse muscle was found to differ from that of rat muscle by having a major nonsaturable component.At all external creatine concentrations, entry of creatine into dystrophic muscles exceeded entry into normal muscles, even after correcting for a greatly expanded inulin space in dystrophic muscles. This finding is inconsistent with the hypothesis of inhibited creatine entry in vivo, leaving accelerated loss of creatine to explain the low creatine content of skeletal muscle of dystrophic mice.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
