Changes in Adrenocorticotropic Hormone(ACTH)Release from the Cultured Anterior Pituitary Cells of Streptozotocin-Induce Diabetic Rats
書誌事項
- タイトル別名
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- Changes in Adrenocorticotropic Hormone (ACTH) Release from the Cultured Anterior Pituitary Cells of Streptozotocin-Induced Diabetic Rats.
- Changes in Adrenocorticotropic Hormone
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説明
We examined ACTH release from cultured anterior pituitary cells of streptozotocin (STZ)-induced diabetic rats. Rats 1 week after the injection of STZ (55 mg/kg, i.v.) were used as a short-terms diabetic model, while rats 8 weeks after the injection of STZ were used as a long-term diabetic model. ACTH release induced by corticotropin-releasing factors (CRF) was significantly increased in the short-term diabetic rats, whereas ACTH release decreased in the long-term diabetic rats. A stimulator of adenylate cyclase, forskolin, caused marked increases in ACTH release in short-term diabetic rats, whereas it did not affect the long-term diabetic rats. An L-type Ca2+ channel agonist, BAY K 8644, did not affect ACTH release in the short-term diabetic ras, although it decreased ACTH release in long-term diabetic rats. In addition, CRF-induced ACTH release also increased in normal anterior pituitary cells cultured under high glucose conditions (25 mmol/l) for 5d.These results suggest that the increase in teh CRF-induced ACTH release from cultured anterior pituitary cells of short-term diabetic rats appears to involve the cAMP system in part. In contrast, the decrease in the CRF-induced ACTH release from the cultured anterior pituitary cells of long-term diabetic rats may indicate a change in the properties of the L-type Ca2+ channel coupled with the CRF receptor, or in the CRF receptor itself.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 21 (8), 795-799, 1998
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282679598095360
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- NII論文ID
- 110003639464
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 4547600
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- PubMed
- 9743244
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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- PubMed
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- 使用不可