| Project/Area Number |
09671078
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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 |
内分泌・代謝学
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| Research Institution | Institute of Gerontology, Nippon Medical School |
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Principal Investigator |
MINAMI Shiro Nippon Medical School Institute of Gerontology Professor, 老人病研究所, 教授 (10192361)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | growth hormone / ultradian rhythm / androgen / somatostatin / growth hormone-feleasing factor / hypothalamus / feedback regulation |
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| Research Abstract |
Growth hormone (GH) secretion is regulated by two hypothalamic hormones, somatostatin and Gil releasing factor (GRE), and markedly episodic in mammals. The secretory pattern of Gil is determined by the reciprocal secretion of these hypothalamic hormones, which are also regulated by many factors. Among these, modulatory effect of androgen to somatostatin release and autofeedback regulation of GH itself are important. The purposes of the present studies are to examine whether androgen induces structural changes to masculinize Gil secretory pattern, and whether the induction of the expression of the c-fos gene is modulated by andregen. The secretory pattern of Gil in ovariectomized female rats was masculinized to male pattern by subcutaneous injection 0.1-1.0 mg diliydrotestosterone (DHT), and 1.0 mg DHT converted GH secretory pattern within 6 hours after the injection. The immediate effect of transient exposure of androgen indicate that Gil secretory pattern was masculinized without changes of the neural structure. The patterns of induction of the c-fos gene in the hypothalamus were not different between hypophysectomizeci male and female rats. However, the estradiol administration reduced c-fos gene expression, whereas DHT did not. The data indicate that autofeedback regulation
by Gil itself to the hypothalamus is also modulated by sex steroids.
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