Détermination par Immunohistochime de zones du système nerveux central impliquées dans l’effet satiétogène de protéines

Faipoux, Rodolphe; Tomé, Daniel; Gougis, S.; Bensaïd, Albert; Prudhomme, Michelle; Oriol, Esther; Fromentin, Gilles

doi:10.1016/s0007-9960(04)94414-8

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“…Palatability has a major impact on the reward system but the expression of liking cannot alone explain the anorexigenic effect of proteins ( 36 ) . Proteins inhibit the activation of opioid and GABAergic neurons in the NAcc and thus could inhibit food intake by reducing the hedonic response to food ( 103 ) . It is well known that neurons in the AccSh project directly to the lateral hypothalamic area ( 104 ) and the stimulation of orexigenic lateral hypothalamic area neurons can induce robust feeding ( 105 ) .…”

Section: Protein-induced Reduction In Eating and Central Neuronal Patmentioning

confidence: 99%

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

et al. 2012

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The present review summarises current knowledge and recent findings on the modulation of appetite by dietary protein, via both peripheral and central mechanisms. Of the three macronutrients, proteins are recognised as the strongest inhibitor of food intake. The well-recognised poor palatability of proteins is not the principal mechanism explaining the decrease in high-protein (HP) diet intake. Consumption of a HP diet does not induce conditioned food aversion, but rather experience-enhanced satiety. Amino acid consumption is detected by multiple and redundant mechanisms originating from visceral (during digestion) and metabolic (inter-prandial period) sources, recorded both directly and indirectly (mainly vagus-mediated) by the central nervous system (CNS). Peripherally, the satiating effect of dietary proteins appears to be mediated by anorexigenic gut peptides, principally cholecystokinin, glucagon-like peptide-1 and peptide YY. In the CNS, HP diets trigger the activation of noradrenergic and adrenergic neurons in the nucleus of the solitary tract and melanocortin neurons in the arcuate nucleus. Additionally, there is evidence that circulating leucine levels may modulate food intake. Leucine is associated with neural mechanisms involving mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK), energy sensors active in the control of energy intake, at least in the arcuate nucleus of the hypothalamus. In addition, HP diets inhibit the activation of opioid and GABAergic neurons in the nucleus accumbens, and thus inhibit food intake by reducing the hedonic response to food, presumably because of their low palatability. Future studies should concentrate on studying the adaptation of different neural circuits following the ingestion of protein diets.

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Section: Protein-induced Reduction In Eating and Central Neuronal Patmentioning

confidence: 99%

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

et al. 2012

View full text Add to dashboard Cite

show abstract

Détermination par Immunohistochime de zones du système nerveux central impliquées dans l’effet satiétogène de protéines

Cited by 1 publication

References 0 publications

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

Peripheral and central mechanisms involved in the control of food intake by dietary amino acids and proteins

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