Premium
Inhibition of gastric motility induced by intestinal glucose in awake rats: role of Na + ‐glucose co‐transporter
Author(s) -
RAYBOULD H. E.,
ZITTEL T. T.
Publication year - 1995
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1111/j.1365-2982.1995.tb00203.x
Subject(s) - glucose transporter , motility , transporter , perfusion , medicine , carbohydrate , chemistry , endocrinology , intestinal motility , small intestine , gastric emptying , carbohydrate metabolism , biology , biochemistry , stomach , insulin , microbiology and biotechnology , gene
Carbohydrates are a component of chyme that initiate feedback control of gastric emptying. The aim of the study was to investigate the mechanism by which sensors in the intestine are activated by carbohydrate to initiate intestinal feedback of gastric motor function. Intestinal perfusion with D‐glucose inhibited gastric motility in awake rats. This response was reproduced by 3‐0‐methyl glucose, a non‐metabolizable analogue of glucose that is absorbed by the Na + ‐glucose co‐transporter, but not by 2‐deoxy‐D‐glucose, and was attenuated by perfusion of the intestine with phloridzin, a competitive blocker of the Na + ‐glucose co‐transporter. Feeding a high carbohydrate diet to increase the number of co‐transporters reduced the response to intestinal glucose. It was concluded that activation of sensors to initiate feedback inhibition of gastric motility may be dependent either on rapid accumulation of glucose within epithelial cells or on activation of the Na + ‐glucose co‐transporter.