title: 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.
  
  
  OBJECTIVE
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Applied Biosciences, Research Faculty of Agriculture, Hokkaido University, Kita-9, Nishi-9, Kita-ku, Sapporo 060-8589, Japan. hira@chem.agr.hokudai.ac.jp
authors.forename: Tohru
authors.initials: T
authors.lastname: Hira
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Maekawa
authors.forename: Kozo
authors.initials: K
authors.lastname: Asano
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hara
mesh_terms: D000818:Animals; D052179:Antigens, Plant; D002118:Calcium / Q000502:physiology; D002460:Cell Line; D002614:Chelating Agents / Q000494:pharmacology; D002766:Cholecystokinin / Q000378:metabolism*; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000037:antagonists & inhibitors / Q000502:physiology*; D005916:Globulins / Q000737:chemistry / Q000494:pharmacology*; D051379:Mice; D055099:Neuroendocrine Cells / Q000187:drug effects* / Q000378:metabolism* / Q000502:physiology; D010456:Peptides, Cyclic / Q000494:pharmacology; D010461:Peptones / Q000494:pharmacology*; D055314:Seed Storage Proteins / Q000737:chemistry / Q000494:pharmacology*; D015398:Signal Transduction; D030262:Soybean Proteins / Q000737:chemistry / Q000494:pharmacology*
chemical_list: D052179:Antigens, Plant; D002614:Chelating Agents; D005916:Globulins; D010456:Peptides, Cyclic; D010461:Peptones; D055314:Seed Storage Proteins; D030262:Soybean Proteins; C475455:YM-254890; C013894:beta-conglycinin protein, Glycine max; C070379:1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; D004533:Egtazic Acid; D002766:Cholecystokinin; D043802:GTP-Binding Protein alpha Subunits, Gq-G11; D002118:Calcium