1994 Fiscal Year Final Research Report Summary
Analysis of the mechanism in the onset of diabetes : the relationship between intracellular signal transduction and DNA damage.
| Project/Area Number |
04807175
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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 | University of the Ryukyus, Faculty of Medicine (1994)
Shinshu University (1992-1993) |
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Principal Investigator |
KOMIYA Ichiro University of the Ryukyus, Faculty of Medicine, Associate Professor, 医学部・付属病院・第2内科, 助教授 (50162061)
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| Co-Investigator(Kenkyū-buntansha) |
TAKASU Nobuyuki University of the Ryukyus, Faculty of Medicine, Professor, 医学部・第2内科, 教授 (20020927)
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| Project Period (FY) |
1992 – 1994
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| Keywords | Diabetes mellitus / Signal transduction / Intracellular Ca^<2+> / Nitric oxide (NO) / Apoptosis / DNA damage |
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| Research Abstract |
(1) Ionomycin and caffeine induced the first phase of insulin secretion from rat perfused pancreas. This was affected by basal glucose concentration and did not induced in low concentration of glucose.
(2) L-arginine, a potent insulin secretogogue, did not induce Ca^<2+> efflux in the study of ^<45>Ca, even if basal glucose concentration was increased. Since the Ca efflux was definitely induced by glucose, arginine and glucose thought to induce insulin secretion in the differnt manner each other.
(3) Arginine vasopression (AVP) and Angiotensin II increased intracellular Ca^<2+> and then induced insulin secretion from rat perfused pancreas and perfused rat islets. The insulin secretion was dependent on the basal glucose concentration of perfusate. Since the effect of AVP was inhibited by V_1-antagonist, and did not inhibted by V_2-antagonist, that was induced through the increase of intracellular Ca_<2+>.
(4) D-glucose induced nitric oxide (NO) production from rat perfused pancreas, but there was time lag between No production and insulin secretion. These data suggested that NO production from the pancreas was related to cell damage, and not related to insulin secretion directly.
(5) Streptozotosin induced apoptosis of rat pancreas islets. The relationship between apoptosis and NO production is now investigated.
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