Abstract
Recently we reported ‘myogenic hyperuricemia’ in muscle glycogenosis types III, V and VII (Kono et al., 1986; Kono et al., 1987; Mineo et al., 1985; Mineo et al., 1987). The mechanism of myogenic hyperuricemia is: when energy production does not fill its requirement for continuing exercise, purine nucleotide degradation is accelerated (Fig. 1). The degradation of purine nucletide occurs even with mild exercise in these diseases. Its degradative metabolites such as inosine, hypoxanthine, and ammonia are released from working muscles into blood stream. Inosine and hypoxanthine are taken up by liver and metabolized to uric acid, causing hyperuricemia. In this study, we report exercise-induced alteration of erythrocyte glycolysis in muscle glycogenoses(Fig. 1), which is another metabolic consequence caused by accelerated purine nucleotide degradation in muscle.
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© 1989 Plenum Press, New York
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Shimizu, T. et al. (1989). Exercise Induced Alteration of Erythrocyte Glycolysis Associated with Myogenic Hyperuricemia. In: Mikanagi, K., Nishioka, K., Kelley, W.N. (eds) Purine and Pyrimidine Metabolism in Man VI. Advances in Experimental Medicine and Biology, vol 253A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5673-8_61
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DOI: https://doi.org/10.1007/978-1-4684-5673-8_61
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