Cholecystokinin secretion induced by beta-conglycinin peptone depends on Galphaq-mediated pathways in enteroendocrine cells.

Abstract:

BACKGROUND:Intraduodenal administration of peptone prepared from soybean beta-conglycinin (BconP) stimulates cholecystokinin (CCK) secretion from enteroendocrine cells, and suppresses food intake in rats. However, the sensing mechanism of BconP by CCK-producing cells is unknown. AIM OF THE STUDY:We investigated signal transduction pathways mediating CCK secretion in response to BconP in the murine CCK-producing cell line, STC-1. METHODS:STC-1 cells were seeded in 48-well culture plates until sub-confluent and CCK secretion was examined under various conditions. CCK concentration was determined by the enzyme immunoassay. RESULTS:BconP dose-dependently induced CCK secretion in STC-1 cells. Treatment with BAPTA-AM, an intracellular Ca2+ chelator, reduced BconP-induced CCK secretion, however, removal of extracellular Ca2+ did not affect the secretory response. Treatment with 2-amino borate (2-APB) reduced CCK releasing responses, suggesting the involvement of IP(3). In addition, BconP failed to induce CCK secretion after treatment with the Galphaq protein inhibitor (YM-254890). CONCLUSION:These results indicate that Galphaq pathway is responsible for BconP-induced CCK secretion in STC-1 cells, and suggest the involvement of a Galphaq-coupled GPCR(s) in dietary peptide sensing in enteroendocrine cells.

journal_name

Eur J Nutr

authors

Hira T,Maekawa T,Asano K,Hara H

doi

10.1007/s00394-008-0764-1

subject

Has Abstract

pub_date

2009-03-01 00:00:00

pages

124-7

issue

2

eissn

1436-6207

issn

1436-6215

journal_volume

48

pub_type

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