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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #161389
Title: THE EFFECT OF AROMATIC AMINO ACID SUPPLEMENTATION ON PROTEIN METABOLISM IN EDEMATOUS MALNUTRITION SYNDROME.

Author
item REID, MARVIN - UNIV. OF THE WEST INDIES
item BADALOO, ASHA - UNIV. OF THE WEST INDIES
item FORRESTER, TERRENCE - UNIV. OF THE WEST INDIES
item Jahoor, Farook

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 3/14/2003
Publication Date: 3/14/2003
Citation: Reid, M.E., Badaloo, A.V., Forrester, T.E., Jahoor, F. 2003. The effect of aromatic amino acid supplementation on protein metabolism in edematous malnutrition syndrome. Journal of Federation of American Societies for Experimental Biology. 17: A870.

Interpretive Summary: Not required.

Technical Abstract: We investigated whether supplementation with an aromatic amino acid cocktail (AAA) consisting of (0.5 mmol each of phenylalanine, tryptophan and tyrosine) compared with isonitrogenous amounts of alanine (ALA) would improve measures of protein kinetics in 15 (8 with AAA, 7 ALA) children with edematous malnutrition (aged 6-24 mo) during the acute malnourished state. Supplementation started immediately after the baseline experiment, 2 days post-admission and continued to the end of the acute phase of treatment (second experiment~11 days post-admission). We measured leucine (leu) kinetics, phenylalanine (phe) flux, urea flux by a 10 hr prime continuous infusion of 2H3 'leucine intragastrically, 13C-leucine, 15 N-urea, and 2H5 phenylalanine intravenously in the fed state. Values are mean post-supplementation differences (AAA-ALA) with standard errors adjusted for baseline measurements. There was a trend towards an overall stimulation of protein metabolism in the AAA group with the rate of leucine appearance from protein breakdown being significantly higher suggesting that intake of AAA in the early phase of treatment is deficient, thereby limiting optimal protein turnover rates.