Food intake is controlled by stimuli acting at the pre- and postabsorptive levels. Preabsorptively, nutrients present in the stomach and intestine elicit signals contributing to meal-ending satiety. Neurally mediated signals and hormonal signals both seem instrumental in the production of this gastrointestinal satiety. Postabsorptively, metabolic receptors in the liver that sense the oxidation of metabolic fuels seem to play an important role in the control of post-meal satiety and meal initiation. These receptors are apparently connected with the brain by vagal afferents, because hepatic vagotomy eliminates the effects of various metabolites and metabolic inhibitors on food intake. Glucoreceptors in the hindbrain that sense the utilization of glucose are probably also involved in control of meal initiation. Finally, humoral factors reflecting the size of the fat depots may also function as feedback signals in the control of feeding.