title: Gamma-aminobutyric acid secreted from islet beta-cells modulates exocrine secretion in rat pancreas.
abstract: OBJECTIVE
  To investigate the role of endogenous gamma-amino-butyric acid (GABA) in pancreatic exocrine secretion.
  
  
  METHODS
  The isolated, vascularly perfused rat pancreas was employed in this study to eliminate the possible influences of extrinsic nerves and hormones. Cholecystokinin (CCK; 10 pmol/L) was intra-arterially given to stimulate exocrine secretion of the pancreas.
  
  
  RESULTS
  Glutamine, a major precursor of GABA, which was given intra-arterially at concentrations of 1, 4 and 10 mmol/L, dose-dependently elevated the CCK-stimulated secretions of fluid and amylase in the normal pancreas. Bicuculline (10 micromol/L), a GABA(A) receptor antagonist, blocked the enhancing effect of glutamine (4 mmol/L) on the CCK-stimulated exocrine secretions. Glutamine, at concentrations of 1, 4 and 10 mmol/L, dose-dependently increased the GABA concentration in portal effluent of the normal pancreas. The effects of glutamine on the CCK-stimulated exocrine secretion as well as the GABA secretion were markedly reduced in the streptozotocin-treated pancreas.
  
  
  CONCLUSIONS
  GABA could be secreted from beta-cells into the islet-acinar portal system after administration of glutainine, and could enhance the CCK-stimulated exocrine secretion through GABA(A) receptors. Thus, GABA in islet beta-cells is a hormone modulating pancreatic exocrine secretion.
authors.affiliation: Department of MedicoLife Science, Youngdong University, Chungbuk, Korea.
authors.forename: Yong-Deuk
authors.initials: YD
authors.lastname: Park
authors.forename: Zheng-Yun
authors.initials: ZY
authors.lastname: Cui
authors.forename: Guang
authors.initials: G
authors.lastname: Wu
authors.forename: Hyung-Seo
authors.initials: HS
authors.lastname: Park
authors.forename: Hyoung-Jin
authors.initials: HJ
authors.lastname: Park
mesh_terms: D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002766:Cholecystokinin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D018756:GABA Antagonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D005973:Glutamine / Q000494:pharmacology; D050417:Insulin-Secreting Cells / Q000737:chemistry / Q000378:metabolism* / Q000502:physiology; D008297:Male; D046790:Pancreas, Exocrine / Q000737:chemistry / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011963:Receptors, GABA-A / Q000032:analysis / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism* / Q000502:physiology*
chemical_list: D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D011963:Receptors, GABA-A; D005973:Glutamine; D005680:gamma-Aminobutyric Acid; D002766:Cholecystokinin; D001640:Bicuculline