| Project/Area Number |
09671066
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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 | Yokohama City Univercity |
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Principal Investigator |
SEKIHARA Hisahiko Medical School, Yokohama City Univercity, Professor, 医学部, 教授 (80126094)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Takashi Medical School, Yokohama City Univercity, Associate Professor, 医学部, 助教授 (70168392)
SATO Shinobu Hospital of Medical School, Yokohama City Univercity, Assistant Professor, 医学部・附属病院, 講師 (80244424)
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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 |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | adrenal endrogen / dehydroepiandrosterone / DHEA / hypoglycemic action / insulin resistance / glucose-6-phosphatase / fructose-1.6-bisphosphatase / デヒドロエビアンドロステロン / インスリン / GLUT4 / 糖新生 |
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| Research Abstract |
Adrenal androgen, dehydroepiandrosterone(DHEA) was reported to decrease blood glucose levels in diabetic db/db mice by Coleman et al.in 1982. As no confirming data has not yet been reported since then, we started the present research work by evaluating the action of DHEA.DHEA truly decreased high blood glucose levels in db/db mice. To elucidate the mechanism of the action of DHEA, we evaluated further the activities of gluconeogenic and glycolytic enzymes in the liver and muscle. The activities of glucose- 6-phosphatase(G6Pase) and fructose-1.6-bisphosphatase(FBPase) were increased in db/db mice and DHEA suppressed the increased activities of G6Pase and FBPase. Probably, DHEA suppressed gluconeogenesis by inhibiting the actions of these enzymes. Therefore, DHEA is considered to be a new agent which ameliorates insulin resistance. The actions of DHEA were confirmed in Zucker fatty rats and normal rats.
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