| Project/Area Number |
62570526
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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 | Nippon Medical School |
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Principal Investigator |
WAKABAYASHI Ichiji Department of Medicine, Nippon Medical School, 助教授 (10096662)
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| Co-Investigator(Kenkyū-buntansha) |
SUGIHARA Hitoshi Department of Medicine, Nippon Medical School, 医学部, 助手 (60183414)
MINAMI Shiro Department of Medicine, Nippon Medical School, 医学部, 助手 (10192361)
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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 |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1988: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1987: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Somatostatin / Growth Hormone-releasing factor / -endorphin / hypothalamic deafferentation / B-endorphin / 成長ホルモン |
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| Research Abstract |
The effects of alpha-methyl-p-tyrosine (alpha-MT) and an antiserum specific to rat GRF on GH secretory profile during a 6h continuous infusion of human GRF [1-44]NH_2 were observed in unrestrained abult male Wistar rats. When an antiserum specific to rat GRF was administered, episodic GH secretion was abolished. In these rats, pulsatile GH secretion indistinguishable from that of control rats was resumed in the continuous presence of human GRF. Although alpha-MT inhibited episodic GH secretion, alpha-MT treated rats exhibited high frequency, low-amplitude episodic GH secretion and elevated baseline levels during the stimulation. Since GH sercetion to GRF is determined largely by somatostatin (SS), the results suggest that phasic release of SS plays an important role in determining the rythmicity of episodic GH secretion, and that it is modulated by alpha-MT but not by the immunoneutral ization of GRF.
To examine the characteristics of GH secretion following the termination of the infusi
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on of SS, unrestrained abult female Wistar rats were subjected to repeated infusions of SS separated by 30-min control periods. The magnitude of the rebound GH secertion was dependent on a dose and duration of the exposure. When an antiserum to rat GRF was injected iv 10min befor the cessation of SS infusion, the peak amplitude of rebound GH secretion was reduced to less than 20% of that of control rats. These results suggest that at least part of the influence of SS on GH secretion was exerted at the level of the hypothalamus through modulating the release of GRF.
In rats performed anterolateral hypothalamic deafferentation of the hypothalamus (ALC), characteristic episodic GH pulses were difficult to identify on visual appraisal and baseline plasma GH levels became significantly higher than those of sham operated rats. The plasma GH response to -endorphin was not observed in ALC rats, while the response to GRF did not differ from that of control rats. The amount of GH secreted during 6h was significantly reduced in ALC rats as compared to that of sham operated rats. When ALC rats were subjected to repeated infusions of SS, a large rebound of GH secretion was observed after the removal and the amount of GH secreted during 6h became comparable to that of sham operated rats. Our data dupports the hypotesis that GRF stimulates GH secretion tonically while SS is a primary regulator governing the dynamics of GH secretory activity. Less
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