Assimilation of N¹⁵-histidine in amino acid imbalance

An 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.

Name thesis:degree_name

Ph. D.

Level thesis:degree_level

doctoral

Department dc:contributor.department

Biochemistry and Nutrition

Grantor dc:publisher

Virginia Polytechnic Institute

Year dc:date.issued

1966

Author dc:creator

• Hartman, David Robert

Statement dc:rights

• In Copyright

Licence dc:rights.uri

• http://rightsstatements.org/vocab/InC/1.0/

Language dc:language.iso

en

Handle dc:identifier.uri

http://hdl.handle.net/10919/87653

OAI identifier oai:identifier

oai:vtechworks.lib.vt.edu:10919/87653