An intragastric meal releases the putative satiety factor cholecystokinin from hypothalamic neurons in cats.
The release of cholecystokinin-like immunoreactivity (CCK-LI) from feline hypothalamus was studied in relation to a meal by use of the push-pull perfusion technique. While levels of CCK-LI in the perfusate of overnight-fasted anesthetized cats were below assay sensitivity (less than 7 pg/30 min), intragastric administration of a carbohydrate-amino acid meal elicited a 3-fold increase in CCK-LI, identified by high-performance liquid chromatography as the C-terminal octapeptide of CCK (CCK-8). Examination of an extrahypothalamic site showed no comparable release in CCK-LI. Intravenous infusions of CCK-8 at doses imitating physiological blood levels up to 400 times higher than those seen after physiological stimulation demonstrated the existence of a CCK blood-brain barrier in the lateral hypothalamus. These observations provide support that CCK may play a physiological role in termination of feeding behavior.
D000818:Animals; D002415:Cats; D002766:Cholecystokinin / Q000032:analysis / Q000378:metabolism*; D002851:Chromatography, High Pressure Liquid; D004750:Enteral Nutrition; D005260:Female; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009474:Neurons / Q000502:physiology*; D010477:Perfusion; D012527:Satiation / Q000187:drug effects; D012528:Satiety Response / Q000187:drug effects; D012844:Sincalide / Q000494:pharmacology; D013997:Time Factors
D002766:Cholecystokinin; D012844:Sincalide