European journal of nutrition · 2008
Cholecystokinin secretion induced by beta-conglycinin peptone depends on Galphaq-mediated pathways in enteroendocrine cells.
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Hira Tohru, Maekawa Toshihiro, Asano Kozo, Hara Hiroshi
Аннотация
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.
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.