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Acute and chronic high protein meals activate neuronal pathways in brainstem and hypothalamic areas involved in satiety in rats
Author(s) -
Faipoux Rodolphe,
Tomé Daniel,
Gougis Sylvette,
Darcel Nicolas,
Fromentin Gilles
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a176-d
Subject(s) - cholecystokinin , hypothalamus , anorexia , medicine , endocrinology , arc (geometry) , arcuate nucleus , brainstem , solitary tract , melanocortin , food intake , nucleus , neuropeptide , biology , neuroscience , receptor , geometry , mathematics
The relationship between the satiety induced by high protein meals and activation of brain areas involved in satiety onset remains incompletely understood. We monitored neuronal pathways in brain centres known to be activated by a meal including the Nucleus of the Tractus Solitary (NTS) and the Arcuate Nucleus of the Hypothalamus (Arc) receiving information from gastrointestinal tract and from the blood, respectively. In the NTS, compared to a normal protein diet, acute or chronic intake of a high protein diet increased activation of the noradrenergic/adrenergic pathway known to be involved in cholecystokinin (CCK) induced satiety, but not the Glucagon Like Peptide 1 (GLP‐1) pathway, which is triggered during aversive‐induced anorexia. In the ARC, the melanocortin pathway also presented a greater activation after acute or chronic intake of high protein meals. Taken together, these results indicated that the potency of high protein meals in inhibiting food intake was occurring along with the activation of several specific brain neural pathways involved in satiety and not in aversive behaviour.