| Project/Area Number |
01570926
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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 |
Obstetrics and gynecology
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| Research Institution | Mie University |
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Principal Investigator |
TOYODA Nagayasu Mie University Hospital Assistant Professor, 医学部附属病院, 講師 (40126983)
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| Co-Investigator(Kenkyū-buntansha) |
ICHIO Takao Mie University Hospital Instructor, 医学部附属病院, 助手 (90184605)
YOSHIMURA Koichi Mie Univ. Sch. of Med. Instructor, 医学部, 助手 (50210761)
杉山 陽一 三重大学, 医学部, 教授 (30093131)
村田 和平 三重大学, 医学部, 講師 (50115739)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1989: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Tyrosine Kinase / Insulin / Pregnancy / Insulin receptor / Insulin resistance / チロシンキナ-ゼ / ラット / 骨格筋 |
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| Research Abstract |
[Aim] Late gestation is associated with insulin resistance, Which has been suggested to be due to the impairment of postbinding signal transduction processes. In order to determine the site of the impairment, tyrosine kinasa activity of insulin receptors from pregnant rats was assessed.
[method] Crude membrane fraction was obtained from the homogenates of skeletal muscle or liver of pregnant rats near term. Insulin receptors were partially purified by applying the solubilized crude membrane on the wheat germ agglutinin column. Autophosphorylation of insulin receptors were assessed as follows. The purified insulin receptors was incubated with insulin and [32P]ATP, immunoprecipitated with anti-insulin receptor antibodies, and then separated by SDS polyacrylamide gel electrophoresis. The radioactivity of the separated insulin receptor beta subunit was counted in a scintillation counter. Phosphorylation of exogenous substrates were assessed using poly (Glu4 : Tyr1).
[results] Insulin-stimulated phosphorylation of insulin receptors and exogenous substrates were reduced by 50% in pregnant rats, when equal quantities of insulin binding capacities were compared.
[comments] Impaired tyrosine kinase activity may be a causc for insulin resistance during late pregnancy.
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