title: Inhibition of food intake induced by acute stress in rats is due to satiation effects.
abstract: Acute mild stress induces an inhibition of food intake in rats. In most studies, the cumulative daily food intake is measured but this only provides a quantitative assessment of ingestive behavior. The present study was designed to analyze the reduction in food intake induced by acute stress and to understand which behavioral and central mechanisms are responsible for it. Two different stressors, restraint stress (RS) and forced swimming stress (FSS), were applied acutely to male Wistar rats. We first measured corticosterone and ACTH in plasma samples collected immediately after acute RS and FSS in order to validate our stress models. We measured food intake after RS and FSS and determined meal patterns and behavioral satiety sequences. The expressions of CRF, NPY and POMC in the hypothalamus were also determined immediately after acute RS and FSS. The rise in corticosterone and ACTH levels after both acute RS and FSS validated our models. Furthermore, we showed that acute stress induced a reduction in cumulative food intake which lasted the whole day for RS but only for the first hour after FSS. For both stressors, this stress-induced food intake inhibition was explained by a decrease in meal size and duration, but there was no difference in ingestion speed. The behavioral satiety sequence was preserved after RS and FSS but grooming was markedly increased, which thus competed with, and could reduce, other behaviors, including eating. Lastly, we showed that RS induced an increase in hypothalamic POMC expression. These results suggest that acute stress may affect ingestive behavior by increasing satiation and to some extent by enhancing grooming, and this may be due to stimulation of the hypothalamic POMC neurons.
authors.affiliation: INRA, UMR914 Nutrition Physiology and Ingestive Behavior, F-75005 Paris, France.
authors.forename: J
authors.initials: J
authors.lastname: Calvez
authors.forename: G
authors.initials: G
authors.lastname: Fromentin
authors.forename: N
authors.initials: N
authors.lastname: Nadkarni
authors.forename: N
authors.initials: N
authors.lastname: Darcel
authors.forename: P
authors.initials: P
authors.lastname: Even
authors.forename: D
authors.initials: D
authors.lastname: Tomé
authors.forename: N
authors.initials: N
authors.lastname: Ballet
authors.forename: C
authors.initials: C
authors.lastname: Chaumontet
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000235:genetics; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D004195:Disease Models, Animal; D004435:Eating / Q000502:physiology*; D005106:Exploratory Behavior; D005247:Feeding Behavior / Q000502:physiology*; D005786:Gene Expression Regulation / Q000502:physiology; D008297:Male; D009478:Neuropeptide Y / Q000235:genetics / Q000378:metabolism; D011333:Pro-Opiomelanocortin / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical / Q000379:methods; D012527:Satiation / Q000502:physiology*; D013315:Stress, Psychological / Q000378:metabolism / Q000503:physiopathology*; D013550:Swimming / Q000523:psychology; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D009478:Neuropeptide Y; D012333:RNA, Messenger; D011333:Pro-Opiomelanocortin; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone