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KMID : 0811720030070000193
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Korean Journal of Physiology & Pharmacology
2003 Volume.7 No. 0 p.193 ~ p.0
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γ-Aminobutyric Acid (GABA) in Islet β-Cells Enhnaces Cholecystokinin (CCK) Action in Exocrine Secretion of Isolated, Perfused Rat Pancreas
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Park Yong-Deuk
Cui Zheng-Yun
Park Hyoung-Jin
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Abstract
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GABA is synthesized in pancreatic islet β-cells. Exogenous GABA enhances CCK-evoked pancreatic exocrine secretion. The endocrine part is functionally connected with the exocrine part via islet-acinar portal system. Thus, this study was aimed to see effects of endogenous GABA on pancreatic exocrine secretion. CCK (10 pM) increased secretions of fluid and amylase of the rat pancreas, which was isolated and vascularly perfused with modified Krebs-Henseleit solution. When glutamine, a major precursor of GABA, was given intra-arterially at 1, 4 and 10 mM, not only the CCK-stimulated secretions of fluid and amylase but also GABA secretion determined in portal effluent were dose-dependently elevated in the normal pancreas. Bicuculline (10μM), a GABAA receptor antagonist, blocked the glutamine (4 mM)-enhanced CCK-stimulated pancreatic exocrine secretions. However, glutamine (4 mM) failed to modify the CCK-stimulated exocrine secretions as well as the GABA secretion in the streptozotocin-treated pancreas. Therefore, it is concluded that GABA is secreted by glutamine from islet β-cells into the islet-acinar portal system of the rat pancreas. Endogenous GABA enhances the CCK-stimulated exocrine secretion via GABAA receptors. The results indicate that GABA in islet β-cells is a hormone, which enhances CCK-stimulated pancreatic exocrine secretion.
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KEYWORD
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GABA, Pancreatic exocrine secretion, CCK, Islet β-cells, Glutamine
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