EFFECTS OF GROWTH HORMONE AND CORTICOTROPIN ON METABOLISM OF N15FROM GLYCINE, L-ALANINE, AND AMMONIUM CITRATE1

Abstract

Metabolism of approximately 20 mg. amounts of N15 added to a complete diet as labeled glycine, L-alanine, or ammonium citrate, was studied in normal bitches during nitrogen equilibrium, storage induced by growth hormone, and loss induced by corticotropin. During induced nitrogen storage, excretion of N15 from each of the 3 sources decreased, but the fall was 25, 12, and 9% of the intake respectively for N15 from glycine, alanine, and ammonium citrate. Such preferential utilization supports the concept that growth hormone stimulates anabolic processes; it is difficult to explain on the basis of interference with urea formation. An increase in utilization of N15 from glycine was particularly noteworthy in the present experiments. During induced nitrogen loss, output of N15 from each of the 3 sources rose. The rise was 10 and 24% of the intake respectively, for N15 from glycine and alanine, indicating vigorous catabolism of the latter in experiments with corticotropin. The partititon of excreted N15 yielded no evidence that nitrogen catabolism was qualitatively altered by growth hormone or corticotropin. During storage and loss, the expected relationship between urea N15 and total N15 output was maintained; the minute amount of isotope excreted in creatinine did not change significantly. Growth hormone increased the amount of N15 from all sources that was excreted as ammonia, presumably by increasing incorporation of ingested N15 into precursors of urinary ammonia. Incorporation of Nl5 into fibrinogen reached a maximum in 12-24 hours. When the dietary source was glycine, incorporation was large, and essentially the same during nitrogen equilibrium, induced storage, or induced loss. Incorporation of N15 from alanine or ammonium citrate increased after growth hormone and decreased after corticotropin, but these changes were small.