Neurological dissociation of gastrointestinal and metabolic contributions to meal size control.

Abstract

A method was developed to separate gastrointestinal (GI) and metabolic contributions to meal size and applied to intact and chronic decerebrate (CD) rats. The effect of a 10-ml milk diet preload or 24 hr of food deprivation on the consumption of a 0.1-M sucrose solution was compared with intake in a no-deprivation/no-preload condition. In the no-deprivation/no-preload condition, rats were given their normal complement of feedings but had the contents of their stomachs removed via a gastric cannula before the intake test. Compared with the no-deprivation/no-preload condition, intact and CD rats consumed significantly less after the preload, but only intact rats ate more after deprivation. Thus intact rats were sensitive to both GI and metabolic influences on intake, whereas CD rats responded to only the GI manipulation. The experiments showed that GI and metabolic contributions to the deprivation response are mediated by neural structures that are at least partly nonoverlapping. The GI component is likely to be contained within the caudal brainstem. The neural systems required for the response to the metabolic changes accompanying deprivation appear to be more widely distributed.