Free Amino Acid Pools and Their Role in Regulation

Munro, Hamish N.

doi:10.1016/b978-0-12-510604-7.50012-8

Cited by 194 publications

(79 citation statements)

References 343 publications

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“…The plasma threonine curve followed a pattern similar to that described by Lewis and Speer (1974) Plasma threonine ratios before and after feeding were greater than one for the four higher dietary threonine levels while the lowest of threonine levels fed resulted in a ratio less than one. A similar response was reported by Meisinger and Speer (1979) with tryptophan deficient diets and is considered indicative of an amino acid de ficiency (Longenecker and Hause, 1959;Munro, 1970).…”

Section: Death Lossmentioning

confidence: 56%

Threonine Requirement for Reproduction in Swine

Leonard¹,

Speer²

1983

Journal of Animal Science

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Section: Death Lossmentioning

confidence: 56%

Threonine Requirement for Reproduction in Swine

Leonard¹,

Speer²

1983

Journal of Animal Science

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“…Thus, induction of tryptophan pyrrolase does cause a general depletion of tryptophan stores within the animal. The fall in concentration was greatest for skeletal muscle which comprises 45% of the total body weight (Munro, 1970). Therefore, the greatest decline in the non-protein tryptophan content will occur within muscle.…”

Section: Resultsmentioning

confidence: 99%

“…Presumably much of the tryptophan that is catabolized is newly released from labile protein stores in response to the administration of hydrocortisone, which has a primarily catabolic action (Munro, 1964). Much of the labile protein in the rat is in the liver, which rapidly synthesizes protein while amino acids are being absorbed from the digestive system, and then catabolizes the protein and releases amino acids in the post-absorptive state (Munro, 1970). Tryptophan is the least abundant amino acid in the pool available for protein synthesis and tryptophan levels play some role in regulating protein synthesis in the liver (Munro, 1970).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of Decline in Rat Brain 5‐hydroxytryptamine After Induction of Liver Tryptophan Pyrrolase by Hydrocortisone: Roles of Tryptophan Catabolism and Kynurenine Synthesis

Young

1981

British J Pharmacology

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1 Two mechanisms have been proposed to explain the decline in brain tryptophan and 5-hydroxytryptamine (5-HT) after administration of hydrocortisone and the subsequent induction of liver pyrrolase. These are depletion of tryptophan by high rates of tryptophan catabolism and inhibition of tryptophan uptake by elevated levels of the tryptophan catabolite, kynurenine.2 The increase in plasma kynurenine after hydrocortisone injection (25 mg/kg) was small, and kynurenine, at a concentration ten fold greater, did not inhibit tryptophan uptake by brain as measured by the Oldendorf technique. Thus, inhibition of tryptophan uptake by kynurenine is not an important mechanism in the control of brain tryptophan and 5-HT. 3 The decline in brain tryptophan after hydrocortisone was comparable to that seen in other tissues, which comprise more than half of the body weight of a rat. 4 The total decline in free tryptophan stores in whole animals treated with hydrocortisone was estimated to be about 450 pg. This amount of tryptophan would be catabolized by tryptophan pyrrolase in about 20 min, when the enzyme is induced, according to an earlier estimate of the rate of tryptophan catabolism in vivo. 5 Tryptophan pyrrolase activity remains high for much longer than 20 min, suggesting that there is net protein catabolism, which releases tryptophan and prevents non-protein tryptophan levels falling very far. 6 These results demonstrate that the decline in brain tryptophan and 5-HT after hydrocortisone is caused by depletion of tryptophan stores due to the high activity of tryptophan pyrrolase. However, our data suggest that this effect is diminished by release of tryptophan from proteins. Thus, peripheral protein metabolism may be an important factor in the control of brain tryptophan levels and 5-HT synthesis.

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“…Les différences artério-veineuses mammaires de glucose dépendent linéairement des taux artériels de glucose lorsque la plage de variation de ceux-ci est très étendue (Linzell, 1960 (Linzell, 1960) (Munro, 1970 …”

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