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Effects of Arginine-Free Meals on Ureagenesis in Cats

  • P. M. Stewart
  • M. Batshaw
  • D. Valle
  • M. Walser
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 153)

Summary

Cats given a single arginine-free meal have been reported to develop severe hyperammonemia, attributed to impaired function of ornithine aminotransferase (OAT). We found that cats which developed hyperammonemia following an arginine-free meal had low hepatic ornithine levels. However, the average sum of hepatic ornithine plus arginine plus citrulline rose, indicating that some ornithine synthesis via OAT took place, and hyperammonemia failed to occur in cats with higher hepatic ornithine levels. OAT activity and kinetic constants were comparable to values reported in the rat. Furthermore, dietary supplementation with ornithine caused only occasional and transient hyperornithinemia. Thus, OAT can function in the cat. The Ka of N-acetylglutamate (AGA) synthetase for arginine was five times higher in cats than in rats, but AGA content and citrullinogenesis by intact mitochondria were the same following arginine-free or arginine-containing meals. Other kinetic parameters of AGA synthetase and carbamylphosphate synthetase were similar to values in the rat. We conclude that low levels of hepatic ornithine are probably responsible for making some cats susceptible to hyperammonemia following this stimulus.

Keywords

Kinetic Parameter Dietary Supplementation Kinetic Constant Impaired Function Urea Cycle 
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.

Copyright information

© Springer Science+Business Media New York 1982

Authors and Affiliations

  • P. M. Stewart
    • 1
  • M. Batshaw
    • 1
  • D. Valle
    • 1
  • M. Walser
    • 1
  1. 1.Johns Hopkins University School of MedicineBaltimoreUSA

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