1995 Fiscal Year Final Research Report Summary
Studies on physiological function of GAD and GABA in pancreatic islet
| Project/Area Number |
06671032
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Kobe University |
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Principal Investigator |
TANIGUCHI Hiroshi Kobe University, School of Medicine, Professor, 医学部, 教授 (70030989)
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| Project Period (FY) |
1994 – 1995
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| Keywords | GAD / GABA / Pancreatic islet / Physiological function |
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| Research Abstract |
The physiological function of gamma-aminobutyric acid (GABA) decarboxylase (GAD) and its synthesizing GABA in pancreatic islets is studied by comparing the GABA level of islets with that of central nervous tissues in terms of responsiveness to drugs affecting GAD and GABA transaminase (GABA-T) , a metabolizing enzyme of GABA,and by observing the effect of some insulin release stimulators on GAD level in islets.
(1) Studies in vivo
(a) The intraperitoneal administration of 3-mercaptopropionic acid known to suppress GAD in central nervous tissues into Wistar rats decreased the GABA content in the hypocampus, hypothalamus, superior colliculus and striatum as well as in islets.
(b) The similar injection of sodium valproate known to suppress GABA-T in central nervous tissues raised the GABA content in all abovementioned tissues.
(2) Studies in vitro
(a) Incubation of isolated Wistar rat islets with 3-mercaptopropionic acid or sodium valproate decreased or increased the GABA content in the islets respectively.
(b) GAD level measured with Western blot in islets did not change by arginine which does not stimulate insulin synthesis but increased by glucose which stimulates insulin synthesis.
These observations indicate that GAD as well as GABA-T are apparently similar in terms of pharmacological response between the central nervous tissues and the islets, and that the GAD in islets seems to play a role in insulin synthesis.
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Research Products
(17 results)
