D-glucose releases 5-hydroxytryptamine from human BON cells as a model of enterochromaffin cells

2001 ◽  
Vol 121 (6) ◽  
pp. 1400-1406 ◽  
Author(s):  
Minsoo Kim ◽  
Helen J. Cooke ◽  
Najma H. Javed ◽  
Hannah V. Carey ◽  
Fievos Christofi ◽  
...  
Keyword(s):  
Enterochromaffin Cells ◽  
Bon Cells

scholarly journals UTP – Gated Signaling Pathways of 5-HT Release from BON Cells as a Model of Human Enterochromaffin Cells

2017 ◽  
Vol 8 ◽  
Author(s):  
Andromeda Liñán-Rico ◽  
Fernando Ochoa-Cortes ◽  
Alix Zuleta-Alarcon ◽  
Mazin Alhaj ◽  
Esmerina Tili ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Enterochromaffin Cells ◽  
Bon Cells

Mechanical stimulation of human BON cells: Gαq involvement in 5-HT release

2001 ◽  
Vol 120 (5) ◽  
pp. A83-A83
Author(s):  
M KIM ◽  
N JAVED ◽  
F CHRISTOFI ◽  
H COOKE
Keyword(s):  
Mechanical Stimulation ◽  
Bon Cells ◽  
Stimulation Of

Synthesis and secretion of atrial natriuretic peptide by BON cells: Stimulation by PMA and cGMP

2001 ◽  
Vol 120 (5) ◽  
pp. A682-A682
Author(s):  
W GOWERJR ◽  
G CARTER ◽  
C LANDON ◽  
W GOWERIII ◽  
J DIETZ ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Bon Cells ◽  
Atrial Natriuretic

Enterochromaffin cells of the rat duodenal mucosa

1976 ◽  
Vol 81 (5) ◽  
pp. 758-759
Author(s):  
E. S. Starkova ◽  
B. T. Anufriev
Keyword(s):  
Duodenal Mucosa ◽  
Enterochromaffin Cells

scholarly journals FFA2 activation combined with ulcerogenic COX inhibition induces duodenal mucosal injury via the 5-HT pathway in rats

2017 ◽  
Vol 313 (2) ◽  
pp. G117-G128 ◽  
Author(s):  
Yasutada Akiba ◽  
Koji Maruta ◽  
Kazuyuki Narimatsu ◽  
Hyder Said ◽  
Izumi Kaji ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Short Chain Fatty Acids ◽  
Serotonin Release ◽  
Enterochromaffin Cells ◽  
Bicarbonate Secretion ◽  
Rat Duodenum ◽  
Free Fatty Acid Receptor ◽  
Small Intestinal

Serotonin (5-HT), predominantly synthesized and released by enterochromaffin cells, is implicated in gastrointestinal symptoms such as emesis, abdominal pain, and diarrhea. Because luminal short-chain fatty acids (SCFAs) release 5-HT from enterochromaffin cells, which express the SCFA receptor free fatty acid receptor 2 (FFA2) in rat duodenum, we examined the effects of the selective FFA2 agonist phenylacetamide-1 (PA1) on duodenal 5-HT release with consequent bicarbonate secretion [duodenal bicarbonate secretion (DBS)] and on indomethacin (IND)-induced enteropathy. Intestinal injury was induced by IND (10 mg/kg sc) with or without PA1. We measured DBS in vivo in a duodenal loop perfused with PA1 while measuring 5-HT released in the portal vein. Duodenal blood flow was measured by laser-Doppler flowmetry. IND induced small intestinal ulcers with duodenal sparing. PA1 given with IND (IND + PA1) dose dependently induced duodenal erosions. IND + PA1-induced duodenal lesions were inhibited by the FFA2 antagonist GLPG-0974, ondansetron, or omeprazole but not by RS-23597 or atropine. Luminal perfusion of PA1 augmented DBS accompanied by increased portal blood 5-HT concentrations with approximately eight times more release at 0.1 mM than at 1 µM, with the effects inhibited by coperfusion of GLPG-0974. Luminal PA1 at 1 µM increased, but at 0.1 mM diminished, duodenal blood flow. Cosuperfusion of PA1 (0.1 mM) decreased acid-induced hyperemia, further reduced by IND pretreatment but restored by ondansetron. These results suggest that, although FFA2 activation enhances duodenal mucosal defenses, FFA2 overactivation during ulcerogenic cyclooxygenase inhibition may increase the vulnerability of the duodenal mucosa to gastric acid via excessive 5-HT release and 5-HT3receptor activation, implicated in foregut-related symptoms such as emesis and epigastralgia.NEW & NOTEWORTHY Luminal free fatty acid receptor 2 agonists stimulate enterochromaffin cells and release serotonin, which enhances mucosal defenses in rat duodenum. However, overdriving serotonin release with high luminal concentrations of free fatty acid 2 ligands such as short-chain fatty acids injures the mucosa by decreasing mucosal blood flow. These results are likely implicated in serotonin-related dyspeptic symptom generation because of small intestinal bacterial overgrowth, which is hypothesized to generate excess SCFAs in the foregut, overdriving serotonin release from enterochromaffin cells.

Fe II uptake of enterochromaffin Biochemical and histochemical study of the ferrous ion uptake reaction in relation to enterochromaffin cells and mast cells

1978 ◽  
Vol 61 (2) ◽  
pp. 248-256 ◽  
Author(s):  
Ralph D. Lillie ◽  
Patricia T. Donaldson ◽  
Philip Pizzolato ◽  
Columbia Reynolds ◽  
Shitalkumar Jirge
Keyword(s):  
Mast Cells ◽  
Histochemical Study ◽  
Enterochromaffin Cells ◽  
Ion Uptake ◽  
Ferrous Ion
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