Effect of ammonia via prepyriform cortex on regulation of food intake in the rat

Noda, Kazutaka; Chikamori, Kazumasa

doi:10.1152/ajplegacy.1976.231.4.1263

Cited by 32 publications

(14 citation statements)

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“…1 and 2) inhibits hunger mechanisms and leads to weight loss. An additional more direct link between hyperammonemia and feeding behavior was reported by Noda and Chikamori who observed reductions in food intake after ammonium chloride injections into the prepyriform cortex (35). Thus, hyperammonemia may lead to reductions in food intake by direct or indirect actions on cerebral satiety control centers.…”

Section: Discussionmentioning

confidence: 84%

Cerebral glucose metabolism after portacaval shunting in the rat. Patterns of metabolism and implications for the pathogenesis of hepatic encephalopathy.

et al. 1986

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The regional cerebral metabolic rate for glucose was measured in normal and portacaval shunted rats and the effects of unilateral carotid infusions of "threshold" amounts of ammonia were assessed. 8 wk after shunting the glucose metabolic rate was increased in all 20 brain regions sampled. Effects on subcortical and phylogenetically older regions of the brain were most pronounced with a 74% increase observed in the reticular formation at the collicular level. Increases in the cerebral cortex ranged from 12 to 18%. Unilateral infusions of ammonia did not affect behavior but altered the electroencephalogram and selectively increased the glucose metabolic rate in the thalamus, hypothalamus, and substantia nigra in half ofthe animals, a pattern similar to that seen after a portacaval shunt, suggesting hyperammonemia as the cause of postshunt increases in glucose metabolism. Visual inspection of autoradiograms, computed correlation coefficients relating interregional metabolism, and principal component analysis suggest that normal cerebral metabolic and functional interrelationships are altered by shunting. Ammonia stimulation of the hypothalamic satiety centers may suppress appetite and lead to cachexia. Reductions in the ammonia detoxification capacity of skeletal muscle may increase the probability of developing future episodes of hyperammonemia, perpetuating the process. Direct effects of ammonia on specific brain centers such as the dorsomedial hypothalamus and reticular activating system may combine with global disruptions of cerebral metabolic-functional relationships to produce the protean manifestations of portal-systemic encephalopathy.

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Section: Discussionmentioning

confidence: 84%

Cerebral glucose metabolism after portacaval shunting in the rat. Patterns of metabolism and implications for the pathogenesis of hepatic encephalopathy.

et al. 1986

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“…ROGERS and LEUNG (1973) suggested that the prepyriform cortex and medial amygdala are involved in the response of rats to diets low in, or devoid of, a single essential amino acid, but not those high in leucine or protein. NODA and CHIKAMORI (1976) demonstrated that ammonia acting on the prepyriform cortex may play a role in depressing food intake due to amino acid imbalanced diet.…”

Section: Discussionmentioning

confidence: 99%

Constancy of net protein intake in rats on self-selection regimen with proteins of various qualities.

et al. 1982

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Voluntary intake of proteins of various qualities in relation to dietary protein utilization was investigated in growing and adult rats. The rats were given two diets, one containing high protein and the other no protein, and were allowed to self-select protein and energy intakes freely from both diets. The results showed that total food intake (protein diet plus protein-free diet) and body weight gain were similar among five proteins tested. However, the amount of protein consumed by the growing rats per 100 g of total food intake (i.e., dietary protein level) was different depending upon the protein qualities, that is, wheat gluten (WG) 44 g, casein (CA) 30 g, soy protein (SP) 21 g, lactalbumin (LA) 19 g, and amino acid mixture simulating egg protein (AA) 11 g. Net protein utilization (NPU), estimated as the proportion of protein intake that is retained in the body, was as follows : WG, 20 %; CA, 33 %; SP, 44 %; LA, 50 %; and AA, 74 %. From the above figures, net dietary protein value, which is a measure of utilizable protein in the diet, was calculated by multiplying the dietary protein level by NPU. In contrast to the difference in protein intake, net dietary protein value was quite constant in spite of large differences in the dietary protein quality, being 8 to 10 %. A similar relationship between protein intake and protein utilization was obtained also with adult rats, except that the net dietary protein value was smaller in adult rats than in growing rats. These results may suggest that the animals can regulate the intake of dietary protein to keep the amount of protein available for the body constant.

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“…This sensory role for the APC is based on the following: (a) ablations of the APC by brain lesions that show its essentiality for detection of IAA deficiency [23–25] (these lesions were replicated in the rat [26], and in the bird [27]), (b) repletion by injecting nanomole amounts of the limiting IAA into the APC to block the anorectic responses [28–30], and (c) electrophysiological measures that show neural activation of the APC in IAA depletion, both in vivo [31] and in vitro [32]. These findings have been reviewed in detail [25, 33–35].…”

Section: Protein and Iaa Deficiencymentioning

confidence: 99%

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

Gietzen

Aja

2012

Mol Neurobiol

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The essential (indispensable) amino acids (IAA) are neither synthesized nor stored in metazoans, yet they are the building blocks of protein. Survival depends on availability of these protein precursors, which must be obtained in the diet; it follows that food selection is critical for IAA homeostasis. If even one of the IAA is depleted, its tRNA becomes quickly deacylated and the levels of charged tRNA fall, leading to disruption of global protein synthesis. As they have priority in the diet, second only to energy, the missing IAA must be restored promptly or protein catabolism ensues. Animals detect and reject an IAA-deficient meal in 20 min, but how? Here, we review the molecular basis for sensing IAA depletion and repletion in the brain’s IAA chemosensor, the anterior piriform cortex (APC). As animals stop eating an IAA-deficient meal, they display foraging and altered choice behaviors, to improve their chances of encountering a better food. Within 2 h, sensory cues are associated with IAA depletion or repletion, leading to learned aversions and preferences that support better food selection. We show neural projections from the APC to appetitive and consummatory motor control centers, and to hedonic, motivational brain areas that reinforce these adaptive behaviors.

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Effect of ammonia via prepyriform cortex on regulation of food intake in the rat

Cited by 32 publications

References 0 publications

Cerebral glucose metabolism after portacaval shunting in the rat. Patterns of metabolism and implications for the pathogenesis of hepatic encephalopathy.

Cerebral glucose metabolism after portacaval shunting in the rat. Patterns of metabolism and implications for the pathogenesis of hepatic encephalopathy.

Constancy of net protein intake in rats on self-selection regimen with proteins of various qualities.

The Brain's Response to an Essential Amino Acid-Deficient Diet and the Circuitous Route to a Better Meal

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