| Project/Area Number |
13671148
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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 |
Endocrinology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TAKANO Koji The University of Tokyo, Faculty of Medicine, research associate, 医学部附属病院, 助手 (20236243)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | Ghrelin / Grow hormone / Channel / alectrophysiology / secretion / Ghrelin / channel / electro physiology / secretion / ghrelin(グレリン) / 成長ホルモン / イオンチャネル / 電気生理学 / 非選択性腸イオン電流 / 細胞内カルシウム濃度 / ホルモン分泌 |
|---|
| Research Abstract |
The mechanism of ghrelin-induced excitation of human GH-secreting cells was investigated using perforated- whole cell clamp technique and measurement of intracellular Ca^<2+> concentration [Ca^<2+>]I. Ghrelin depolarized GH-secreting human pituitary adenoma cells and increased action potential frequency. The depolarization was induced by a Na^+ influx through nonselective cation channels. The signal transduction of ghrelin-induced activation of the nonselective cation current involved protein kinase C. Ghrelin increased intracellular Ca^<2+> concentration of these cells depending mainly on the Ca^<2+> influx through the voltage-gated Ca^<2+> channels. This Ghrelin-induced increase in [Ca^<2+>]I was abolished in Na^+-free extracellular solution but was not abolished by tetrodotoxin, indicating that the ghrelin-induced cation current and depolarization are important in ghrelin-induced [Ca^<2+>]I increase. Ghrelin increased GH secretion dependency on the voltage-gated Ca^<2+> influx. In non-adenoma human GH-secreting cells, ghrelin-induced activation of a nonselective cation current and depolarization was also observed. These data indicate that ghrelin stimulates GH secretion by excitating these cells and increasing Ca^<2+> influx through the voltage-gated Ca^<2+> channels in human GH-secreting cells.
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