| Project/Area Number |
62440065
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Sapporo Medical College |
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Principal Investigator |
KUMAMOTO Yoshiaki Sapporo Medical College,Professor, 医学部, 教授 (40045323)
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| Co-Investigator(Kenkyū-buntansha) |
ITOH Naoki Sapporo Medical College,Instructor, 医学部, 助手 (60193504)
UMEHARA Tsugio Sapporo Medical College,Instructor, 医学部, 助手 (90160324)
TSUKAMOTO Taiji Sapporo Medical College,Associate Professor, 医学部, 助教授 (50112454)
高木 良雄 札幌医科大学, 医学部, 助手 (50154761)
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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 |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥7,000,000 (Direct Cost: ¥7,000,000)
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| Keywords | Male infertility / Secretion capacity / Spermatogenesis / E2 / T ratio / Transferrin / inhibin / LH |
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| Research Abstract |
We analyzed clinically and experimentally causes of male infertility. The clinical investigation aimed to clarify an influence of testicular estrogen on spermatogenesis, and of Sertoli cell function evaluated by seminal plasma transferrin and inhibin on seminalysis findings and treatment efficacy. We also investigated a significance of FSH and testosterone in the treatment for male infertility with elucidating the effect of these hormones on rat spermatogenesis.
1. An analysis of E2/T ratio changes in 24 hour hCG test revealed the poorer thera-peutic efficacy in patients with more than 3.5 of E2/T increasing ratio than those with 3.5 or less. The further study identified a higher E2 increasing rate in such patients. These findings suggested that patients with the enhancing E2 secretion capacity. The hormone treatment would not give a satisfactory result. The unfavorable result could be explained in part by a direct or indirect action of E2 on steroidogenesis or on suppression of testicu
… More
lar function through a negative feedback mechanism upon hypothalamus-pituitary system, respectively.
2. Both seminal tranferrin and inhibin had a negative correlation to sperm count, indicating that these would be useful marker to evaluate a Sertoli cell function. This finding was supported by that these markers showed a significant decrease in patients with severe hypospermatogenesis in histological examination of testis.
3. We also performed an experimental study using medical hypophysectomized rat produced by high dosis-administration of LH-RH analogue. This experiment implied an important role of testosterone in meiotic phase and of FSH in spermatid maturation. The presence of testosterone would be crucial especially in differentiation from spermatocyte to spermatid.
These results described above have led us to conclusion that an enhancing secretion of testicular estrogen caused an inhibition on testosterone synthesis and its normal action, which resulting in hypospermatogenesis. Further efforts will be necessary on a measurement of seminiferous androgen and androgen receptor, as well as an evaluation of E2 changes during treatment. Less
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