1997 Fiscal Year Final Research Report Summary
Effect of Growth hormone on the translocation of GLUT4 and its relation to insulin-like and anti-insulin action
| Project/Area Number |
08670895
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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 |
Pediatrics
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| Research Institution | Tokushima University |
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Principal Investigator |
YOKOTA Ichiro Department of Pediatrics, Tokushima University Hospital Research Associate, 医学部・附属病院, 助手 (50253208)
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| Co-Investigator(Kenkyū-buntansha) |
KURODA Yasuhiro Department of Pediatrics, Tokushima University School of Medicine Professor, 医学部, 教授 (20035471)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Growth Hormone / GLUT4 / Insulin-like action / Insulin resistance / Akt kinase |
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| Research Abstract |
To elucidate the effect of growth hormone (GH) on the insulin signal transduction pathway leading to the translocation of glucose transporter-4 (GLUT4), we constructed Chinese hamster ovary cells that overexpressed GH receptor and GULT4. Treatment with GH triggered GLUT4 translocation, and this translocation was completely inhibited by wortmannin. GH-induced GLUT4 translocation reached a maximum level after 30 minutes, and then gradually decreased and returned to the basal level after 2 hours. Tyrosine phosphorylation of JAK2 also became maximal after 30 minutes and then gradually decreased. In contrast, GLUT4 translocation remained unchanged for 2 hours after insulin treatment, and tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) also remained constant for up to 2 hours. Chronic GH treatment had almost no effect on insulin-stimulated Akt kinase activation and GLUT4 translocation. These results suggest that GH and insulin translocate GLUT4 in a similar manner, at least in part, and the difference in translocation depends on the difference in the tyrosine phosphorylation of JAK2 and IRS-1. The anti-insulin action of GH after chronic GH treatment does not appear to be mainly due to the inhibition of GLUT4 translocation.
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