J. Wen et al., PW AND GLP-1 CONTRIBUTE TO FEEDBACK INHIBITION FROM THE CANINE ILEUM AND COLON, American journal of physiology: Gastrointestinal and liver physiology, 32(6), 1995, pp. 945-952
To explore mechanisms whereby unabsorbed nutrients in the ileum inhibi
t the upper gut (''ileal brake''), we perfused the canine ileum or col
on and monitored phase 3 in the duodenum. Easting motility was recorde
d when the ileum or colon was perfused with 154 mM NaCl, a mixed isoto
nic nutrient solution (Ensure), or individual nutrients (maltose, case
in hydrolysates, or sodium oleate). Blood samples were collected befor
e and during the perfusions. The ileum was also perfused with 154 mM N
aCl while peptide YY (PYY) was infused by vein. In both sets of experi
ments, plasma levels of PYY, neurotensin, and glucagon-like peptide-1
(GLP-1) were measured. Ileal or colonic perfusion of Ensure delayed ph
ase 3 [migrating motor complexes (MMC)] in the duodenum, inhibited ile
al motility, and increased plasma levels of PYY and GLP-1. Ileal casei
n and oleate and colonic casein also delayed the duodenal MMC. The MMC
cycle length and plasma levels of PW were closely correlated. Intrave
nous PYY prolonged the MMC cycle; an intravenous dose of 100 pmol . kg
(-1). h(-1) of PW mimicked the effects of ileal Ensure. These results
support the hypothesis that PYY, and possibly GLP-1, participate in th
e ileal brake. This negative feedback loop also affects the distal sma
ll bowel. The proximal colon also triggers the feedback inhibition of
gut motility (colonic brake).