| Project/Area Number |
09671040
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
内分泌・代謝学
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| Research Institution | GIFU UNIVERSITY |
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Principal Investigator |
ISHIZUKA Tatsuo Department of General Medicine, GIFU UNIVERSITY, Professor, 医学部・附属病院, 教授 (20108070)
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| Project Period (FY) |
1997 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Diabetic complication / platelet aggregation / PKC / serotonin release / hypertension / leptin / 糖尿病 / トロンビン / イノシトール隣脂質 代謝 / セロトニン / 高血圧 / PKC阻害剤 / rhoA / 低分子量G蛋白 / 糖尿病性網膜症 / 糖尿病性腎症 / phosphatidy linositol 3-kinase |
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| Research Abstract |
1)Plalelet PKC β immunoreacitivity in cytosol fraction was siguificantly higher in diabetic patients with normal serum creatinine(Cr)level than in diabetic patients with abnormal Cr level(Cr ≧ 15 mg/dl)or in healthy subjects. Platelet PKCβ immunoreactivity in cytosol from diabetic patients treated with sulphonylurea was significantly higher than that from healthy subujects. In addition, PKCβ immunoreactivity in diabetic patients with insulin treatment was significantly suppressed compared to that in patients treated by sulphonylurea treatment. These results suggest that chronic hyperglyecmia may activate platelet PKCβ isoform, and that insulin treatment may decrease platelet PKCβ activity.
2)It has been reported that the presence of hypertension in diabetes causes a decrease in intraplatelet serotonin content. We investigated 0.1 U/ml thrombin-sutimulated[^<14>C]serotonin release from platelet in 17 diabetic subjects. Thrombin-induced serotonin release from platelet in diabetic subjects
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was significantly increased, compared with controls and hypertension without diabetes. Thrombin-induced platelet serotonin release in diabetic patients with hypertension was significantly higher than in diabetic patients without hypertension. There was no significant correlation among the severities of diabetic complication, and diabetic treatment in thrombin-induced serotonin release from 17 diabetic patients. Increased serotonin release from platelet in diabetes may contribute to the development of macroangiopathy in diabetes with hypertension.
3)We studied serum leptin concentration ard agonist-induced platelet aggregation in platelets from 13 diabetic subujects who did not use the medicine which influenced the platelet function, and 9 contorol subjects(6 men, 3 woman, average age 32.4 ±13.6 years old, and average BMI 23.0±2.5 kg/m^2). It was observed positive correlation between the serum leptin concentration and BMI in both diabetic and control subjects. There was no significant difference of serum leptin concentration in diabetic subjects with and withouto diabetic complication. These results suggest that ADP-stimulated maximum platelet aggregation rate may be associated with serum leptin concentration in diabetic subjects. Less
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