Abstract
Luminal nutrient chemosensing during meal ingestion is mediated via intestinal endocrine cells to regulate secretion and motility. We have reported that luminal L‐glutamate (L‐Glu) with inosinate (IMP) stimulates duodenal bicarbonate secretion (DBS) possibly via taste receptor heterodimers T1R1/R3. To further study this mechanism, we hypothesized the involvement of gastric inhibitory peptide (GIP) or glucagon‐like peptide (GLP) release in L‐Glu/IMP‐induced DBS. We measured DBS with a pH‐stat or with pH and CO2 electrodes through a rat duodenal loop. Rat GIP, GLP‐2, or exendin‐4 (GLP‐1 receptor agonist, Ex‐4) was continuously injected iv (0.1 – 1 nmol/kg/hr). Furthermore, L‐Glu and/or IMP was luminally perfused with or without iv injection of ProGIP (GIP receptor antagonist) or exendin‐3‐(9–39) (GLP‐1 receptor antagonist). GIP and GLP‐2 dose‐dependently increased DBS, whereas Ex‐4 decreased DBS. Perfusion of L‐Glu with IMP increased DBS, with no effect of ProGIP or exendin‐3‐(9–39). Luminal perfusion of L‐Glu with IMP increased portal venous [GLP‐1], with no effect on [GIP]. These results suggest that L‐Glu/IMP‐induced DBS is possibly mediated via GLP‐2 release.A grant from Ajinomoto Inc, NIH R01 DK54221
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