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1 Anatomy, Physiology and Cell Biology, UC Davis School Vet Med, Davis, California, United States
* To whom correspondence should be addressed. E-mail: heraybould{at}ucdavis.edu.
The presence of glucose in the intestinal lumen elicits a number of changes in gastrointestinal function including inhibition of gastric emptying and food intake and stimulation of pancreatic and intestinal secretion. The present study tested the hypothesis that SGLT-3, a member of the SGLT family of transport proteins, is involved in detection of luminal glucose in the intestine. Gastric emptying, measured in awake rats, was significantly inhibited by perfusion of the intestine with glucose (60 and 90 mg); this effect was mimicked by 
-methyl glucose (non-metabolizable substrate of SGLT-1 and 3), but not 2-deoxy-D-glucose (substrate for GLUT-2) or iso-osmotic mannitol. Gastric motility and intestinal fluid secretion, measured in anesthetized rats, were significantly inhibited and stimulated, respectively, by duodenal glucose, but not galactose, which has a much lower affinity for SGLT-3 than glucose. Duodenal glucose but not galactose stimulated the release of 5-HT into mesenteric lymph and stimulated the discharge of duodenal vagal afferent fibers. mRNA for SGLT-3 was identified in the duodenal mucosa. Together these data suggest that detection of glucose in the intestine may involve SGLT-3, possibly expressed by enterochromaffin cells in the intestinal mucosa, and release of 5-HT.
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