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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #110961


item Yokoi, Katsuhiko
item Uthus, Eric
item Nielsen, Forrest - Frosty

Submitted to: Great Lakes Regional American Chemical Society Symposium
Publication Type: Abstract Only
Publication Acceptance Date: 3/20/2000
Publication Date: 6/2/2000
Citation: Yokoi, K., Uthus, E.O., Nielsen, F.H. 2000. Supplemental sulfur amino acids (SAA) affect pyridoxine metabolism [abstract]. 32nd Great Lakes 2000 Regional Meeting of the American Chemical Society Abstracts of Presentations. p.17.

Interpretive Summary:

Technical Abstract: The intermediate metabolism of SAA is influenced by dietary pyridoxine and nickel. Pyridoxine deficiency in humans increased circulating homocysteine, which has been associated with ischemic heart disease. Thus, to ascertain whether high dietary SAA changes the need for pyridoxine or its metabolism, a factorially arranged experiment with male Sprague-Dawley rats was performed. Dietary variables were supplemental SAA: none, 10 g dl-methionine (MET)/kg, and 10 g dl-homocystine (HCY)/kg, pyridoxine hydrochloride: 0 and 7.5 mg/kg, and Ni: 0 and 1 mg/kg. Both MET and HCY similarly increased the urinary excretions of inorganic sulfate and ammonia with the molar ratio of 1 sulfate and 2 ammonia, compared to animals without supplemental SAA. Compared to animals without supplemental SAA, HCY increased plasma ammonia and pyridoxal phosphate; MET increased plasma pyridoxal phosphate only for animals without supplemental pyridoxine. These results suggest that SAAs affect pyridoxine metabolism although dietary pyridoxine does not affect SAA catabolism through the main transsulfuration pathway.