| Project/Area Number |
62570504
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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 Tokyo |
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Principal Investigator |
OKA Yoshitomo Faculty of Medicine, University of Tokyo, 医学部(病), 助手 (70175256)
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| Co-Investigator(Kenkyū-buntansha) |
ASANO Tomoichiro Faculty of Medicine, University of Tokyo, 医学部(病), 医員
SHIBASAKI Yoshikazu Faculty of Medicine, University of Tokyo, 医学部(病), 助手 (80196419)
KASUGA Masato Faculty of Medicine, University of Tokyo, 医学部(病), 助手 (50161047)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Glucose transporter / Glucose transporter mRNA / 糖尿病 / 心臓 |
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| Research Abstract |
We raised three antipeptide antibodies against three different domains of HepG2 type glucose transporter. These antibodies recognized only 3 and 30 % of all the glucose transporters presnt in rat adipocyte and brain, respectively, suggesting the presence of more that two types of glucose transporter in rat adipocyte and brain. Western blotting of the brain membranes from streptozotocin-induced diabetic rats with these antibodies showed no difference in the glucose transporter amount, compared with normal rats or insulin-treated diabetic rats. In addition, photoaffinity-labeling of glucose transporter with [^3H] cytochalasin B showed no alteration of glucose transporter amount in the brain from diabetic rats. Furthermore, no significant changes in the amount of HepG2 type glucose transporter mRNA was observed in the brain from diabetic rats when Northern blotting was performed with rabbit brain HepG2 type glucose transporter cDNA as a probe. The similar results were observed in the heart from diabetic rats, i. e. no significant changes were observed in the amount of both glucose transporter protein and HepG2 type glucose transporter mRNA compared with normal rats or insulin-treated diabetic rats.
These results showed a remarkable contrast to the results observed in the adipocytes from diabetic rats, indicating that different mechanisms regulate the amount of glucose transporter in different tissues in diabetic state.
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