ABSTRACT
For CNS 5-HT to be involved in episodic appetite
regulation, it must receive input from the periphery during
and after consumption. These signals can be classified by
their origin (i.e., stimulus and location). During the
prandial phase, the CNS receives postingestive sensory
afferent input from the gut, reflecting both the amount of
food eaten and the earliest representations of its nutrient
content. Firstly, mechanoreceptors in the gut detect the
distension of gut lining caused by the presence of food,
contributing to the estimation of the volume of food
consumed. Secondly, gut chemoreceptors detect the
chemical presence of various nutrients in the gastrointes-
tinal tract providing information on the composition (and
possible energy content) of the food consumed. Finally,
prandial and postprandial signals are generated by the
detection of nutrients that were absorbed from the gastro-
intestinal tract and then entered the circulation in the
periphery (postabsorptive satiety signals). Circulating
nutrients are either metabolized in the periphery (e.g.,
liver) and activate CNS receptors (e.g., in brain stem) or
they enter and affect the brain directly and act as post-
absorptive metabolic satiety signals (2,3). Such afferent
information must ultimately affect CNS 5-HT functioning.
