The alimentary canal, liver and vagus play a role in short-term feeding: but is the role regulation, correlation, glucostasis or spurious association?
The injection of insulin has been used to produce increased food intake and, when given over a period of time, to produce obesity. The hormone, however, is released in 3 distinct phases when subjects encounter and ingest food and one would expect that insulin release would be a correlate, if not a contributory factor, to satiety. On the other hand, glucagon has been used to suppress food intake, but pancreatic glucagon should be released during the absence of food. The present paper investigates the physiologic function of these hormones and gives evidence that insulin serves as part of the normal sequence of hormonal and neural responses to food intake and does appear to play a contributory, causal role in short-term satiety for food intake.
D000818:Animals; D002766:Cholecystokinin / Q000494:pharmacology; D003847:Deoxyglucose / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology; D004435:Eating / Q000187:drug effects*; D005247:Feeding Behavior / Q000187:drug effects*; D005934:Glucagon / Q000494:pharmacology*; D007328:Insulin / Q000494:pharmacology*; D008112:Liver Glycogen / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D014044:Tolbutamide / Q000494:pharmacology; D014630:Vagus Nerve / Q000502:physiology
D007328:Insulin; D008112:Liver Glycogen; D005934:Glucagon; D002766:Cholecystokinin; D014044:Tolbutamide; D003847:Deoxyglucose