| Project/Area Number |
62570520
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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 |
内分泌・代謝学
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| Research Institution | Tokyo Women's Medical College |
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Principal Investigator |
SUDA Toshihiro Dept. of Med. Tokyo women's Med. Coll. Associate Professor, 内科2, 助教授 (30075452)
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| Co-Investigator(Kenkyū-buntansha) |
SUMITOMO Takashi Dept. of Med. Tokyo women's Med. Coll. Assistant
NAKAGAMI Yuriko dept. of Med. Tokyo Women's Med. Coll. Assistant (70188887)
住友 高 東京女子医科大学, 内科2, 助手
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | CRF / ACTH / POMC / Gene-exprssion / Pituitary / 視床下部 / クッシング病 / Corticotropin-releasing factor / POMCmRNA |
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| Research Abstract |
Gene expression of hypothalamic CRF and pituitary proopiomelanocortin (POMC), and characterization of CRF-binding protein (CRF-BP) were examined. The results are as follows; 1. cAMP-related ACTH secretagogues stimulated both ACTH release and POMC gene expression in the pituitary, while protein kinase C-related ACTH secretagogues did not affect POMC gene expression. 2. Insulin-induced hypoglycemia stimulated gene expression of hypothalamic CRF and pituitary POMC as well as secretion of ACTH and CRF in rats. 3. CRF-BP appeared to have a mol wt of about 38000, and its binding to CRF was specific. 4. CRF-BP inhibited CRF-induced ACTH secretion from the pituitary cells. 5. most of the increased plasma CRF formed in pregnant women was bound to CRFBP, and so is inactive.
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