1999
DOI: 10.1006/appe.1999.0242
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Rapid Fall in Plasma Threonine followed by Increased Intermeal Interval in Response to First Ingestion of a Threonine-devoid Diet in Rats

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Cited by 18 publications
(9 citation statements)
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References 35 publications
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“…In conclusion, the utilization of a calibrated 3-g Thr-dev test meal to induce a taste aversion ruled out the possibility that increased levels of plasma ammonia could reach toxic levels and refuted the hypothesis that an increased postprandial metabolism could generate satiety signals. In contrast, ingestion of the Thr-dev test meal induced a rapid and pronounced depression in circulating threonine, a result that confirms that plasma amino acid pattern is rapidly modified in the rat after ingestion of an amino-acid-imbalanced diet (7).…”
Section: Discussionsupporting
confidence: 62%
“…In conclusion, the utilization of a calibrated 3-g Thr-dev test meal to induce a taste aversion ruled out the possibility that increased levels of plasma ammonia could reach toxic levels and refuted the hypothesis that an increased postprandial metabolism could generate satiety signals. In contrast, ingestion of the Thr-dev test meal induced a rapid and pronounced depression in circulating threonine, a result that confirms that plasma amino acid pattern is rapidly modified in the rat after ingestion of an amino-acid-imbalanced diet (7).…”
Section: Discussionsupporting
confidence: 62%
“…This response is independent of food sensory stimuli or peripheral signals (5355) and instead relies on direct neuronal sensing of EAA imbalance by the anterior piriform cortex (APC). This assertion is supported by the following observations: (i) APC lesions prevent rats discriminating between AA containing and AA devoid diets (56, 57), (ii) concentrations of the limiting EAA in the APC rapidly fall after the introduction of the devoid diet (41, 48), through competition at the capillary endothelial amino acid transport system (5860), and (iii) replacement of the limiting EAA into the APC via microinjections rapidly increases intake of a diet deficient in that EAA (49, 57, 61, 62). Importantly, this aversive response was shown to be independent of diet palatability and novelty (63).…”
Section: Central Detection Of Essential Amino Acid Devoid or Unbalancmentioning
confidence: 75%
“…These discrepancies could be explained by diverging experimental paradigms (duration of fast, amino acid composition of the baseline diet) that may affect the production or kinetics of central EAA imbalance (77). In paradigms evidencing a rapid aversive response to EAA imbalance diets, a rapid fall in the APC concentration of the limiting amino acid occurred in the same time course as the production of the hypophagic response, within 40 min of diet exposure (41, 48, 78), and correlated with the activation of the GCN2 pathway in the APC (71, 72). In the Leib study, plasma concentrations of the missing amino acid and APC GCN2 signaling 1 h after diet exposure were unchanged, suggesting that the EAA imbalance failed to reach the APC during early exposure to the diet in these conditions.…”
Section: Central Detection Of Essential Amino Acid Devoid or Unbalancmentioning
confidence: 98%
“…When Leu is supplied in excess, the concentration of Val in plasma is reduced (Langer et al, 2000). This decrease in the most limiting amino acid in the plasma is also observed in the brain and is thought to be the metabolic signal responsible for the anorectic response (Peng et al, 1972;Feurte et al, 1999). BCAA readily pass across the blood-brain barrier (Hargreaves and Pardridge, 1988) and could reach the anterior piriform cortex of the brain, which is thought to host a chemosensor of an amino acid imbalance (Leung and Rogers, 1971).…”
Section: Discussionmentioning
confidence: 99%