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 that 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 K(a) of N-acetylglutamate (AGA) synthetase for arginine was 5 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 carbamoylphosphate 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.
|Original language||English (US)|
|Number of pages||6|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|State||Published - 1981|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Physiology (medical)