Assimilation by Rats of Limiting Amino Acid into Protein from Imbalanced Dietary Sources

Hartman, David; King, Kendall W.

doi:10.1093/jn/92.4.455

Cited by 17 publications

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“…Ribosomal function can also be disrupted by a disproportion of indispensable amino acids-a state which may arise if too much of the diet consists of palatable or readily accessible vegetable foods. The level of deficient amino acid can limit the rate of protein synthesis even though the excess of nonlimiting amino acids can stimulate incorporation at the same time (Benevenga, Harper, & Rogers, 1968;Hartman & King, 1967), possibly via the adrenal activation by which cycloheximide has a similar effect (Jondorf, Simon, & Avnimelech, 1966). On the other hand, Harper, Benevenga, and Wohlheuter (1970) have suggested that generally it is the high plasma levels of non-limiting amino acids that act on behavior, without the protein-synthesis inhibition which is seen in the particular case of tryptophan deficiency (Sidransky, Sarma, Bongiorno, & Verney, 1968;Wunner, Bell, & Munro, 1966).…”

Section: Discussionmentioning

confidence: 99%

Aversion to a cue acquired by its association with effects of an antibiotic in the rat.

Booth¹,

Simson²

1973

Journal of Comparative and Physiological Psychology

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Section: Discussionmentioning

confidence: 99%

Aversion to a cue acquired by its association with effects of an antibiotic in the rat.

Booth¹,

Simson²

1973

Journal of Comparative and Physiological Psychology

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“…The reduction in plasma Tyr levels when the IAA − Phe mixture was added to diets containing high levels of Phe suggests that the availability of Phe as a substrate for PAH may have been reduced by the other indispensable amino acids. Alternatively, the reduction in Tyr concentration may reflect increased use of Tyr in protein synthesis as been reported in imbalances (Yoshida et al, 1966;Hartman and King, 1967;Benevenga et al, 1968;Soliman and King, 1969;Ip and Harper, 1974). The tendency for plasma Tyr concentration to be unchanged when the IAA − Phe supplement was added to the basal diet may be attributable to the presence of Tyr in the IAA − Phe mixture.…”

Section: Plasma Amino Acid Concentrationsmentioning

confidence: 93%

“…A third possibility is that Phe is sequestered as a result of increased protein synthesis. Several studies provide evidence that imbalancing mixtures of indispensable amino acids stimulate hepatic protein synthesis (Yoshida et al, 1966;Hartman and King, 1967;Benevenga et al, 1968;Soliman and King, 1969;Ip and Harper, 1974).…”

Section: Plasma Amino Acid Concentrationsmentioning

confidence: 99%

“…The observed reduction in growth has been attributed to the reduced feed consumption, which in turn may be a consequence of the altered plasma amino acid profile (Leung and Rogers, 1969;Harper et al, 1970;Gietzen et al, 1998). The reduction in the concentration of the limiting amino acid in plasma has been attributed to increased protein synthesis (Yoshida et al, 1966;Hartman and King, 1967;Benevenga et al, 1968;Soliman and King, 1969;Ip and Harper, 1974) and increased catabolism of the first-limiting amino acid Austic, 1982, 1994;Park and Austic, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Phenylalanine hydroxylase activity and expression in chicks subjected to phenylalanine imbalance or phenylalanine toxicity

Lartey

Austic

2009

Poultry Science

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Experiments were performed to investigate the activity of hepatic Phe hydroxylase (PAH) and plasma amino acid concentrations under conditions of Phe imbalance or toxicity in chicks fed on experimental diets from 7 to 14 or 16 d of age. In experiment 1, Phe imbalance was created by adding 10% of a mixture of indispensable amino acids lacking Phe (IAA - Phe) to a basal diet containing 0.46% Phe. The activity of PAH was not significantly affected by the imbalance. Correcting the imbalance by adding 1.12% Phe to the diet prevented the growth impairment and increased the activity of PAH. In experiment 2, growth was reduced by the addition of excess (2%) Phe to the basal diet. Correcting the excess by adding the IAA - Phe to the diet prevented the growth reduction. The activity of PAH was not significantly affected by 2% Phe, but it increased in chicks fed the corrected diet. The levels of PAH mRNA were not affected by the dietary treatments. A factorial arrangement of treatments with 3 dietary levels of Phe (0.46, 1.58, and 2.46%) with or without the IAA - Phe was used in experiment 3. The effects on growth were similar to those of the same treatments in experiments 1 and 2. The addition of Phe significantly increased hepatic PAH activity, but there was no detectable main effect of the IAA - Phe and no interaction. Plasma Phe concentration was increased by dietary Phe and decreased by the IAA - Phe mixture. We conclude that hepatic PAH activity in chicks variably increases in response to Phe or a 10% dietary supplement of indispensable amino acids including Phe but does not increase in response to IAA - Phe when the amino acids are added to a diet that is marginally adequate in Phe. The increased activity does not involve changes in PAH mRNA. The effects of IAA - Phe on plasma Phe concentrations appear to be independent of hepatic PAH activity as measured in vitro.

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“…The most often quoted hypothesis is a direct brain detection of the decrease in the plasma and brain level of the limiting amino acid that usually follows the ingestion of a meal lacking this amino acid (11,12,14). An alternative mechanism could proceed through alterations in postprandial protein turnover, but the ingestion for the first time of a meal deficient in an indispensable amino acid usually failed to induce significant changes in postprandial protein synthesis (15,29). Another hypothesis is that alterations in the postprandial catabolism of amino acids may generate signals sensed in the brain to stop food intake.…”

mentioning

confidence: 99%

Postprandial metabolism and aversive response in rats fed a threonine-devoid diet

Even

Rolland

Feurté

et al. 2000

American Journal of Physiology-Regulatory, Integrative and Comp

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Lack of an indispensable amino acid in the diet induces a rapid reduction in food intake. In this study, we assessed whether the anorectic signal after ingestion of a meal lacking threonine originated from either direct perception of the decrease in plasma threonine or from an indirect effect related to increased postprandial amino acid catabolism and energy expenditure. We observed that 3 g of such a meal was sufficient to induce an aversive response to the diet within 2 h. Postprandial changes to plasma ammonia and urea, urinary urea, and energy metabolism did not differ from those measured after a control meal. In contrast, plasma threonine levels fell within 1 h after the meal. It is concluded that an increase in postprandial energy expenditure is not involved in the anorectic response to eating a threonine-devoid diet. The drop in plasma threonine levels may be a potential signal, but the fact that the decrease in food intake occurred 1 h after the decrease in plasma threonine questions a direct causal relationship.

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Assimilation by Rats of Limiting Amino Acid into Protein from Imbalanced Dietary Sources

Cited by 17 publications

References 0 publications

Aversion to a cue acquired by its association with effects of an antibiotic in the rat.

Aversion to a cue acquired by its association with effects of an antibiotic in the rat.

Phenylalanine hydroxylase activity and expression in chicks subjected to phenylalanine imbalance or phenylalanine toxicity

Postprandial metabolism and aversive response in rats fed a threonine-devoid diet

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