| Project/Area Number |
09671062
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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 | Kagawa Medical University |
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Principal Investigator |
TAKAHARA Jiro Kagawa Medical University, 1st Dept Int Med, Professor, 医学部, 教授 (00033085)
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| Co-Investigator(Kenkyū-buntansha) |
NIIMI Michio Kagawa Medical University, 1st Dept Int Med, Associate Professor, 医学部, 助教授 (80164523)
TOKUDA Michiaki Kagawa Medical University, University Hospital, Research Assosiate, 医学部附属病院, 助手 (00188731)
FUJITA Jiro Kagawa Medical University, 1st Dept Int Med, Research Assosiate, 医学部, 助手 (80209056)
SATO Makoto Kagawa Medical University, 1st Dept Int Med, Research Assosiate, 医学部, 助手 (10215840)
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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 |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | steroid / growth hormone / IGF-I / rat / Iymphocyte / bone mireral / CD4 / CD8 / DEXA法 / コレステロール / フローサイトメトリー |
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| Research Abstract |
Steroids are widely used to treat a variety of clinical conditions, including certain collagen diseases and bronchial asthma. The therapeutic use is however hampered by severe adverse events related to the catabolic effects of steroids. Growth hormone (GH) is a potent anabolic hormone and it might counteract some catabolic effects of steroids. In the present study, the possible effects of GH on dexamethasone (Dex)-induced adverse events including growth retardation, loss of bone meneral content, and hyperlipidemia were examined in rats. Also, the effects of GH on the immune system under steroid excess were investigated. Rats were treated with Dex in comination with human GH for 4 weeks. The rats treated with Dex showed severe growth retardation, loss of bone mineral content, and hyperlipidemia. Dex also inhibited serum insulin-like growth factor (IGF)-I levels in rats. GH had no effect on the Dex-induced growth retardation and hyperlipidemia, but it tended to increase the bone mineral content measured with a dual energy x-ray absorptiometer. GH partially reversed the decrease in serum IGF-I levels in Dex-treated rats. In the immune system, the number of splenic lymphocytes was noticebly decreased by Dex treatment, whereas the ratio of CD4/CD8 assessed by flow cytometric analysis was not altered. Interestingly, GH treatment increased the ratio of CD4/CD8 in Dex-treated rats and this effect was not observed in control rats. Our results suggest that GH therapy may counteract the bone loss induced by steroids. It should be however noted that GH might interfere with the immunosuppressive effects of steroids. This must be consideredd prior to recommending GH therapy in many diseases under chronic steroid excess. Further studies are required to elucidate the molecular mechanisms for anti-steroid effects of GH on the immune system.
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