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Amino acid responses to exercise stress in well-trained racehorses and human athletes are well characterised, but the knowledge of amino acid metabolism during and after exercise in inactive animal species is limited. To study this, plasma amino acid concentrations were measured in previously unexercised pigs which performed two exercise tests on a treadmill with an interval of one week. In general, the changes in amino acids were more pronounced after the second than after the first exercise bout. Alanine, glutamine, phenylalanine and tyrosine were elevated for one hour only after the latter exercise. Twenty-four hours after the second exercise isoleucine, leucine, phenylalanine, tyrosine and valine were increased, but only isoleucine was increased after the first test. These differences between the two tests might be explained by adaptation of the amino acid metabolism after a single exercise bout and suggest that domestic pigs are well suited to study the early effects of exercise.
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The metabolic effects of TPN containing high amounts of amino acids (18 gm N) was evaluated with respect to sulfur amino acid metabolism and protein breakdown in nine severely burned patients. The results were compared to corresponding data from burned patients receiving more moderate amounts of amino acids (9.2 gm N) or isocaloric amounts of carbohydrate and fat. Significantly increased urinary excretion and intracellular muscle tissue concentrations of methionine were found in patients receiving the concentrated amino acid solution, probably reflecting a combined effect of the injury and an increased load of the compound. These patients also showed a reduced oxidation of sulfur amino acids to inorganic sulfate, which may reflect an increased protein synthesis during treatment. A significantly decreased urinary excretion of 3-methyl-histidine and mercaptolactate was found in patients receiving the concentrated amino acid solution, probably reflecting a decreased breakdown of body protein. The findings favor the hypothesis of an anabolic effect of the new amino acid solution in burned patients during the early catabolic phase, but also emphasize the importance of monitoring the amounts of amino acids, e.g., methionine, given.
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Amino acid metabolism in endogenous psychoses has been discussed in relation to monoamine synthesis. There are no consistent findings which prove altered monoamine syntheses to be the primary change. Our finding, which suggests decreased amino acid transport across the blood-brain barrier in schizophrenia, does not necessarily mean an insufficient amino acid supply to the brain. Several lines of investigation have shown the possibility of the involvement of glutamatergic dysfunction in the pathogenesis of schizophrenia. Our recent finding of decreased CSF asparagine concentration in schizophrenia and its positive correlation with the response to neuroleptics may support this hypothesis. Recently, free D-serine, an allosteric agonist on NMDA-receptor, has been reported to exist in the rat brain, suggesting that D-serine is an intrinsic ligand. The pathogeneses of endogenous psychoses might be studied in terms of disturbed metabolism of amino acid, as allosteric regulater of neuro-receptor, as well as neurotransmitter and precursor of monoamines.
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Amino acid metabolism under surgical stress, injury or infection was reviewed from the literature. The glucose-alanine cycle in coupling with branched chain amino acids (BCAA) metabolism plays a central role for gluconeogenesis, in such a catabolic state. Glutamine is as important as alanine for sparing glucose and furthermore for intestinal repair. Changes in plasma amino acid concentration and clearance following hepatectomy are described, and effects of BCAA solution are evaluated. It was suggested that BCAA improved the Fischer ratio by increasing, not only plasma BCAA level, but also AAA clearance.
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Development of acylcarnitine and amino acid profiling using tandem mass spectrometry, and its application for use with dried blood specimens collected on filter-paper cards, has introduced an innovative new technology for detecting inborn errors of fatty acid, organic acid, and amino acid metabolism. From November 1, 1992 through June 30, 1999 we screened more than 700,000 newborns in Pennsylvania, Ohio, North Carolina, and Louisiana. We have prospectively detected 163 inborn errors of metabolism. Eighty-six patients have amino acid metabolism errors. Among them are phenylketonuria, hyperphenylalaninemia, maple syrup urine disease, and several urea cycle disorders. Thirty-two have organic acid metabolism errors, including glutaric aciduria type 1; 3-methylcrotonyl coenzyme A (CoA) carboxylase deficiency, propionic acidemia, methylmalonic acidemia, and 3-hydroxy-3-methylglutaryl-CoA lyase deficiency; and 45 have fatty acid oxidation errors, including 36 with medium-chain acyl-CoA dehydrogenase deficiency. Details of the methodology are presented and the potential of this screening technology is discussed.
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