Abstract

Regulation of food intake consists of two components: control mechanisms: long-term, including energy homeostasis, and short-term, including meal size and intermeal interval. The enteric nervous system (ENS) of the gastrointestinal tract may serve as the first neuronal component communicating satiety signals originating from the gut and acting on the brain. Cholecystokinin (CCK), a satiety hormone secreted by the duodenal I cells, evokes reduction of meal size in various species. In addition, we have shown that exogenous CCK-8, 33 and 58 and endogenous CCK, released by orogastric gavage of the non-synthetic, non-nutrient, trypsin inhibitor camostat increases Fos-like immunoreactivity; a marker for neuronal activation, in one or both components of the ENS (myenteric and submucosal plexuses).

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