| Project/Area Number |
11672163
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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 |
Biological pharmacy
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| Research Institution | Kitasato University (2000)
The University of Tokyo (1999) |
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Principal Investigator |
HOMMA Hiroshi Kitasato University, School of Pharmaceutical Science Professor, 薬学部, 教授 (50190278)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | D-Aspartate / testosterone / Steroidogenic acute regulatory protein / Leydig cells / steroidogenesis / glutamate transporter / human chorionic gonadotropin / テストテロン |
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| Research Abstract |
D-Aspartate (D-Asp) increases human chorionic gonadotropin (hCG)-induced testosterone production in purified rat Leydig cells. Testosterone production was enhanced only in cells cultured with D-Asp for more than 3 h. The increased production of testosterone was well correlated with the amounts of D-Asp incorporated into the Leydig cells, and L-cysteine sulfinic acid, an inhibitor of D-Asp uptake, suppressed both testosterone production and intracellular D-Asp levels. D-Asp, therefore, is presumably taken up into cells to increase steroidogenesis. Intracellular D-Asp probably acts on cholesterol translocation into the inner mitochondrial membrane, the rate-limiting process in steroidogenesis. D-Asp enhances steady-state cellular mRNA and protein levels of Steroidogenic Acute Regulatory protein, which is a key regulatory factor in gonadal and adrenal steroidogenesis to increase the rate-limiting process. D-Asp therefore appears to increase testosterone production in rat Leydig cells by stimulating Steroidogenic Acute Regulatory protein gene expression. To our knowledge, this is the first report demonstrating a direct effect of D-Asp on gene expression in mammalian cells.
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