| Project/Area Number |
59480253
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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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 | Shiga University of Medical Science |
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Principal Investigator |
KOBAYASHI Masashi Shiga University of Medical Science, 医学部, 講師 (80115758)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Ken Shionogi Research Institute, 研究主任
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| Project Period (FY) |
1984 – 1986
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| Project Status |
Completed (Fiscal Year 1986)
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| Budget Amount *help |
¥6,100,000 (Direct Cost: ¥6,100,000)
Fiscal Year 1986: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1985: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1984: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Insulin receptor / Insulin resistance / Kinase activity of beta-subunit / IGF-1 / インスリン作用 |
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| Research Abstract |
We investigated the mechanism of insulin resistance of insulin receptor diseases, Type A,B and C. For Type A, five families were examined and the binding studies of transformed lymphocytes, erythrocytes as well as fibrobalsts from these patients revealed decreased insulin receptor numbers. Decreased kinase activity of beta-subunits were proportional tothe extent of decreased binding. As for Type C, receptor binding and kinase activity of transformed lymphocytes were normal, indicating that the defect was at post-kinase sites.
In Type B, anti-insulin receptor antibody demonstrated various insulin like activity depend on the cell types such as glucose uptake or kunase activity. Thus, antibody's recognition was various depend on the cell types.
Further studies are necessary to elucidate the mechanism of decreased receptor number in Type A and to identify the exact site of insulin resistance in Type C, possibly glucose transporter. To clarify these unkown probelms, gene analysis of insulin receptor and glucose transporter is mandatory.
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