Cholecystokinin as satiety signal.
Already in 1910 Pavlov suggested that appetite was regulated by signals from the gut to hypothalamus. Since Gibbs et al. in 1973 demonstrated that cholecystokinin (CCK) - in contrast to other gut hormones - decreased food intake in rats, great interest has focused upon this substance. A major question now is the significance in man of large doses of CCK administered intraperitoneally in rats. We now know that CCK can act as a signal both via blood (as hormone) or via nerves ( as transmitter). We have recently shown that CCK in man and pig circulates in low concentrations (a few pmol) making blood-borne CCK an unlikely satiety signal. However, we have also shown that CCK nerves are abundant in the gut. This observation raises the possibility that afferent CCK nerves from the gut may transfer satiety signals to the hypothalamus. The recent demonstration that gastric vagotomy abolishes the satiety effect of CCK may support the idea that afferent vagal nerves containing CCK or the related peptide, gastrin, are crucial in appetite regulation.
D000818:Animals; D001665:Binding Sites; D001812:Blood-Brain Barrier; D002766:Cholecystokinin / Q000502:physiology*; D004435:Eating; D005755:Gastrins / Q000502:physiology; D006801:Humans; D012527:Satiation / Q000502:physiology*; D012528:Satiety Response / Q000502:physiology*; D013045:Species Specificity
D005755:Gastrins; D002766:Cholecystokinin