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Analysis of the mechanism in the onset of diabetes : the relationship between intracellular signal transduction and DNA damage.

Research Project

Project/Area Number 04807175
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field 内分泌・代謝学
Research InstitutionUniversity of the Ryukyus, Faculty of Medicine (1994)
Shinshu University (1992-1993)

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)

Co-Investigator(Kenkyū-buntansha) TAKASU Nobuyuki  University of the Ryukyus, Faculty of Medicine, Professor, 医学部・第2内科, 教授 (20020927)
Project Period (FY) 1992 – 1994
Project Status Completed (Fiscal Year 1994)
Budget Amount *help
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1992: ¥1,000,000 (Direct Cost: ¥1,000,000)
KeywordsDiabetes mellitus / Signal transduction / Intracellular Ca^<2+> / Nitric oxide (NO) / Apoptosis / DNA damage / DNAアポトーシス / 細胞内情報伝達異常 / フリーラジカル / DNA / 実験糖尿病
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.

Report

(4 results)
  • 1994 Annual Research Report   Final Research Report Summary
  • 1993 Annual Research Report
  • 1992 Annual Research Report
  • Research Products

    (4 results)

All Other

All Publications (4 results)

  • [Publications] 小宮一郎,高須信行: "催 糖尿病とフリーラジカル" 活性酸素・フリーラジカル. 4. 14-21 (1993)

    • Related Report
      1993 Annual Research Report
  • [Publications] 小宮一郎: "GLUTZと糖尿病発症" 信州医学雑誌. 42. 81-82 (1994)

    • Related Report
      1993 Annual Research Report
  • [Publications] 高須信行,小宮一郎 長沢慶尚,浅輪孝幸,山田隆司: "高濃度ブドウ糖前処置のラット〓ラ氏島インスリン分泌に及ぼす影響-細胞内遊離Ca^+とインスリン分泌-" 糖尿病. 35. 747-753 (1992)

    • Related Report
      1992 Annual Research Report
  • [Publications] 小宮一郎,高須信行: "催糖尿病薬とフリーラジカル" 活性酸素・フリーラジカル. 4. 14-21 (1993)

    • Related Report
      1992 Annual Research Report

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Published: 1992-04-01   Modified: 2016-04-21  

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