Intestinal fat differentially suppresses sham feeding of liquid diets and p
referred gustatory stimuli. Although the behavioral effect is robust, no el
ectrophysiological evidence exists to account for its neural basis. Therefo
re, we investigated the effect of intestinal fat on gustatory coding in the
pontine parabrachial nuclei (PBN) by recording from single neurons in awak
e rats before, during, and after intraduodenal infusions of lipid (Intralip
id; 10 ml, 5 kcal). Intraduodenal lipid did not alter the response profiles
of PEN taste neurons. It did, however, produce an overall decrease in resp
onse magnitude (-16.25%; n = 43), with the largest reduction to sucrose (-3
0%; n = 43). The most pronounced suppression occurred in sucrose-best neuro
ns in response to sucrose (-55%; n = 19), and this effect was largest for t
he sucrose-specific cells (-77%; n = 3). After lipid infusions, nonspecific
neurons in both the sucrose-best and NaCl-best categories also responded l
ess to their best stimulus (sucrose, -46%; n = 16; NaCl, -35%; n = 13). In
contrast, no significant changes were found in NaCl-specific cells in respo
nse to NaCl. All effects appeared with short latency (similar to 5 min) and
were reversible within the time frame of a meal. In controls, duodenal inf
usions of saline did not cause any changes in taste responsiveness. These r
esults suggest that intestinal fat has specific effects on taste coding in
the PEN that may contribute to the intake suppression of palatable food obs
erved in behavioral studies. The similar, short latency of both the behavio
ral and neural effects supports the hypothesis of a preabsorptive site of a
ction.