Hartman, David Robert2019-02-152019-02-151966http://hdl.handle.net/10919/87653An attempt was made to isolate L-N¹⁵-histidine from Escherichia coli cultured in a defined medium containing nitrogen-15 enriched ammonium salts as the only source of nitrogen. Commercially prepared L-N¹⁵-histidine.HC1.H₂0 was used to follow the limiting amino acid in the imbalanced diet in rats fed a chemically-defined imbalanced or corrected diet. Total nitrogen content and atom percent N¹⁵ were determined on the urine, gastrointestinal contents, diet, and the acid-soluble and protein fractions of the liver, kidneys, muscle, gastrointestinal tract, and serum at two, four, and six hours after the onset of feeding. The data were examined for changes in the concentration of N¹⁵ which might cause the imbalance phenomenon {reduced blood levels of the limiting amino acid). It was found that the limiting amino acid was not catabolized at an increased rate and that it was not absorbed or transported at a reduced rate due to the ingestion of an imbalance amino acid mixture. The increased efficiency with which the histidine was found to be incorporated into metabolically active proteins appears to be a primary cause of the reduced blood levels of the limiting amino acid and, therefore, of the imbalance phenomenon. Experimental verification was, therefore, obtained for the first unverified aspect of Harper's (12) thinking about the cause of the reduced appetite that is characteristic of the imbalance phenomenon.56, v leavesapplication/pdfenIn CopyrightLD5655.V856 1966.H35Dissertation