1995 Fiscal Year Final Research Report Summary
Molecular mechanisms of insulin signal transduction and diabetes mellitus
| Project/Area Number |
06454178
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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 |
Pathological medical chemistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
EBINA Yousuke The University of Tokushima, Institute for Enzyme Research, Professor, 酵素科学研究センター, 教授 (00112227)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Takashi The University of Tokushima, Institute for Enzyme Research, Research Associate, 酵素科学研究センター, 助手 (40210009)
HAYASHI Hideki The University of Tokushima, Institute for Enzyme Research, Associate Professor, 酵素科学研究センター, 助教授 (10218589)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Insulin signal transduction / PI3-kinase / GLUT4 translocation / G-proteins |
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| Research Abstract |
Insulin is a unique hormone to decrease blood glucose level, althou there are several hormones which have abilities to increase the conctration of blood glucose. However the GLUT4 translocation which causes rapid decrease of blood glucose level is not triggered only by inuslin but also other growth factors, PDGF and EGF.Using the mutants of PDGF receptor, we concluded that the PI 3-kinase activated by these growth factors is mainly transmitted the signal of the GLUT4 translocation. These findings promoted the elucidation of the molecular mechanisms of GLUT4 translocation.
We next examined the target molecule of GTPgammaS, because the treatment of GTPgammaS tiggered the GLUT4 translocation. We established the clones in which normal on mutant ras, rab, rad proteins are stablely expressed in our cell system, and we examined the effect of the over-expressed G-proteins on the insulin-stimulated GLUT4 translocation. The results indicated that rab, ras, rho and rad is probably not involved in the insulin signaling pathway of GLUT4 translocation. Our recent results suggested that a kind of trimeric G proteins may be involved the GTPgammaS-stimulated GLUT4 translocation, butthis signaling pathway is independent from the insulin signaling pathway.
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