Alteration of CCK-induced satiety in post-Nippostrongylus brasiliensis-infected rats.
In rats, the nematode Nippostrongylus brasiliensis induces an intestinal inflammation, but after the inflammation had resolved and the worm burden eliminated, morphological alterations of the intestinal wall, mainly consisting of mast cell hyperplasia and enteric nerve remodeling, persist for several weeks. Intestinal signals reaching the brain through the vagus nerve and involving neuropeptides such as CCK, play a role in the control of food intake. Our hypothesis was that neuroimmune alterations of the intestine may alter this control. This work was aimed to evaluate whether post-infection alterations of the intestinal wall may affect the satiety effects of CCK and further, the role of mast cells and their mediators, histamine and serotonin, in post-N. brasiliensis-infected rats. In basal conditions, food intake was not different in control and post-infected groups of rats. Post-infected rats were characterized by prolonged satiety effects of both CCK and histamine but not serotonin. The prolonged effect of CCK was reduced when mast cells were previously stabilized by ketotifen, which had no effect per se on food intake. No difference was observed in the increase of food intake induced by CCK-A and CCK-B receptor antagonists in both control and post-infected rats. Mast cell degranulation with compound 48/80 induced severe anorectic effects that lasted for less than 24h in post-infected rats and as long as 6 days in controls. Thus, in our experimental conditions, i.e., within 30-50 days post-N. brasiliensis infection, we observed an enhancement of the anorectic effect of exogenous CCK involving mast cell degranulation and histamine.
Gay
Jérôme
J
Neuro-Gastroenterology and Nutrition Unit, Institut National de la Recherche, Agronomique, 180 chemin de Tournefeuille, BP 3, 31931 Toulouse Cedex, France.
Ressayre
Lucien
L
Garcia-Villar
Rafael
R
Bueno
Lionel
L
Fioramonti
Jean
J
D000818:Animals; D001570:Benzodiazepinones / Q000494:pharmacology; D015550:Cell Degranulation / Q000502:physiology; D002766:Cholecystokinin / Q000494:pharmacology*; D020109:Devazepide / Q000494:pharmacology; D004435:Eating / Q000187:drug effects; D006632:Histamine / Q000494:pharmacology; D006634:Histamine H1 Antagonists / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D007665:Ketotifen / Q000494:pharmacology; D008297:Male; D008407:Mast Cells / Q000502:physiology; D009559:Nippostrongylus; D010671:Phenylurea Compounds / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors; D012528:Satiety Response / Q000187:drug effects*; D012701:Serotonin / Q000494:pharmacology; D017206:Strongylida Infections / Q000503:physiopathology*
D001570:Benzodiazepinones; D006634:Histamine H1 Antagonists; D006727:Hormone Antagonists; D010671:Phenylurea Compounds; D011949:Receptors, Cholecystokinin; D012701:Serotonin; C058121:L 365260; D006632:Histamine; D002766:Cholecystokinin; D020109:Devazepide; D007665:Ketotifen