PMID- 22643031
OWN - NLM
STAT- MEDLINE
DCOM- 20121203
LR  - 20120816
IS  - 1475-2700 (Electronic)
IS  - 0954-4224 (Linking)
VI  - 25
IP  - 1
DP  - 2012 Jun
TI  - Peripheral and central mechanisms involved in the control of food intake by 
      dietary amino acids and proteins.
PG  - 29-39
LID - 10.1017/S0954422411000175 [doi]
AB  - 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.
FAU - Fromentin, Gilles
AU  - Fromentin G
AD  - INRA, CNRH-IdF, UMR914 Nutrition Physiology and Ingestive Behaviour, F-75005 
      Paris, France. gilles.fromentin@agroparistech.fr
FAU - Darcel, Nicolas
AU  - Darcel N
FAU - Chaumontet, Catherine
AU  - Chaumontet C
FAU - Marsset-Baglieri, Agnes
AU  - Marsset-Baglieri A
FAU - Nadkarni, Nachiket
AU  - Nadkarni N
FAU - Tome, Daniel
AU  - Tome D
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20120529
PL  - England
TA  - Nutr Res Rev
JT  - Nutrition research reviews
JID - 9113797
RN  - 0 (Amino Acids)
RN  - 0 (Dietary Proteins)
RN  - 0 (Gastrointestinal Hormones)
RN  - 0 (Neurotransmitter Agents)
SB  - IM
MH  - Amino Acids/*pharmacology
MH  - Appetite Regulation/*drug effects/physiology
MH  - Brain/*drug effects/physiology
MH  - Central Nervous System/drug effects/physiology
MH  - *Diet
MH  - Dietary Proteins/*pharmacology
MH  - Energy Intake/*drug effects/physiology
MH  - Feeding Behavior/*drug effects/physiology
MH  - Gastrointestinal Hormones/metabolism
MH  - Humans
MH  - Neurons/drug effects
MH  - Neurotransmitter Agents/pharmacology
MH  - Satiety Response/drug effects
MH  - Sensation/drug effects
MH  - Taste
EDAT- 2012/05/31 06:00
MHDA- 2012/12/10 06:00
CRDT- 2012/05/31 06:00
PHST- 2012/05/31 06:00 [entrez]
PHST- 2012/05/31 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
AID - S0954422411000175 [pii]
AID - 10.1017/S0954422411000175 [doi]
PST - ppublish
SO  - Nutr Res Rev. 2012 Jun;25(1):29-39. doi: 10.1017/S0954422411000175. Epub 2012 May 
      29.