1999 Fiscal Year Final Research Report Summary
The mechanism of regulation on GnRH pulse generator
| Project/Area Number |
09671704
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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 |
Obstetrics and gynecology
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| Research Institution | Yokohama City University |
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Principal Investigator |
KONDOH Yoshihito Yokohama City University Medical Center Department of Gynecology, Assist. Prof, 医学部・付属病院, 講師 (90244441)
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| Project Period (FY) |
1997 – 1999
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| Keywords | GnRH pulse / stress / Hypothalamic Amenorrhea / Polycystic Ovary Disease / human Corticotropin-Releasing Hormone |
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| Research Abstract |
We investigated the effect of glucose and its related on the recovery of pusatile LH secretion witch suppressed by insulin in estrogen-primed ovariectomised rats and also examined the effect of glucose on the electrical activity of the eGnRH pulse generator. By monitoring the electrical activity of the pulse generator, we found that insulin injection suppressed the pulsatile LH secretion by decreasing the activity of the GnRH pulse generator. Again glucose injection immediately recovered the decrease in the electrical activity of the pulse generator. We suggest that glucose availability is an essential factor for maintaining the electrical activity of the GnRH pulse generator which is responsible for pulsatile LH secretion.
In human, we reported previously that the LH secretary pattern during day and night regressed to pubertal patterns in patients with hypothalamic progestin-negative amenorrhea. We also found that women with functional hypothalamic amenorrhea had a significantly poorer responses of cortisol and ACTH to hCRH than normal women.
In women with PCOS with the high pulse amplitude and basal level of LH, basal plasma ACTH and cortisol were significantly higher and the plasma ACTH after hCRH administration was higher than control. Based on the response to hCRH, patients with PCOS could be classified into 3 types: those with a normal response to hCRH (group 1), those with an exaggerated responses of ACTH to hCRH (group 2), and those with a high basal level of cortisol and a poor response to hCRH (group 3). In groups 2 and 3 dehydroepiandrosterone sulfate was significantly higher, suppression of androstenedione by dexamethasone was significantly greater, and ovulation rates with clomiphene were significantly lower than group 1. This classification provides insight into the underlying cause of PCOS and is thus useful for selection of treatment.
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