Publication

Renal and hepatic nitrogen metabolism during nh4cl ingestion in protein-deprived rats

Lardner, Anne L.
O'Donovan, Daniel J.
Citation
Lardner, Anne L. O'Donovan, Daniel J. (1998). Renal and hepatic nitrogen metabolism during nh4cl ingestion in protein-deprived rats. European Journal of Biochemistry 254 (2), 428-432
Abstract
Three groups of rats were given either a standard protein diet, a protein-free diet, or a protein-free diet with the inclusion of 0.28 M NH4Cl in their drinking water, for 10 days. Body, liver and kidney masses were decreased similarly in the protein-free and protein-free NH4Cl groups. Ingestion of protein-free diet resulted in profound systemic acidosis in both groups, the simultaneous consumption of NH4Cl having no further effect. The activities of the urea-cycle enzymes carbamoyl-phosphate synthease, ornithine transcarbamoylase, arginosuccinate lyase and arginase were significantly reduced in the protein-foe group, and the simultaneous ingestion of NH4Cl had no further effect. These results indicate that ammonium ingestion does not prevent the decrease in urea cycle enzyme activities during a period of dietary-protein deprivation. Renal phosphate-dependent glutaminase activity was unchanged in the protein-free group, but was significantly higher with simultaneous NH4Cl consumption, suggesting that the renal adaptation to acid ingestion is not compromised by a lack of dietary protein. Urinary ammonia excretion also increased in rats consuming protein-free diet and NH4Cl. Urinary urea excretion was greater in rats receiving protein-free diet and NH4Cl than in rats receiving protein-free diet only, at all time-points examined. These data demonstrate that urea synthesis is driven primarily by the need to dispose of protein-derived ammonia rather than bicarbonate.
Funder
Publisher
Wiley-Blackwell
Publisher DOI
10.1046/j.1432-1327.1998.2540428.x
Rights
Attribution-NonCommercial-NoDerivs 3.0 Ireland