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Exercise Induced Alteration of Erythrocyte Glycolysis Associated with Myogenic Hyperuricemia

  • Takao Shimizu
  • Norio Kono
  • Hiroaki Kiyokawa
  • Yuya Yamada
  • Naoko Hara
  • Ikuo Mineo
  • Masanori Kawachi
  • Hiromu Nakajima
  • Yan Lin Wang
  • Masamichi Kuwajima
  • Seiichiro Tarui
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 253A)

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.

Keywords

Uric Acid Serum Uric Acid Serum Uric Acid Level Glycogen Storage Disease Glycolytic Intermediate 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1989

Authors and Affiliations

  • Takao Shimizu
    • 1
  • Norio Kono
    • 1
  • Hiroaki Kiyokawa
    • 1
  • Yuya Yamada
    • 1
  • Naoko Hara
    • 1
  • Ikuo Mineo
    • 1
  • Masanori Kawachi
    • 1
  • Hiromu Nakajima
    • 1
  • Yan Lin Wang
    • 1
  • Masamichi Kuwajima
    • 1
  • Seiichiro Tarui
    • 1
  1. 1.The Second Department of Internal MedicineOsaka University Medical SchoolOsaka, 553Japan

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