INSULIN RELEASE AFTER ACUTE HYDROCORTISONE TREATMENT IN MICE
INSULIN RELEASE AFTER ACUTE HYDROCORTISONE TREATMENT IN MICE
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DOI：
10.1016/0026-0495(83)90031-8
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发表时间：
1983-01-01
影响因子：
9.8
通讯作者：
FLETCHER, HP
中科院分区：
文献类型：
--
作者：
LONGANO, CA;FLETCHER, HP
这项研究探讨了急性剂量氢化可的松琥珀酸钠 (HC) 后抑制胰岛素释放的潜在机制。当给予雄性 Swiss-Webster 小鼠时，氢化可的松 (300 mg/kg i.p.) 会升高血浆葡萄糖水平 (P≤0.05)，但不会改变血浆胰岛素水平。这导致胰岛素生成指数显着降低（P≤0.05）。静脉注射后，氢化可的松抑制了葡萄糖刺激的胰岛素水平（P≤0.05）。进食和禁食小鼠的葡萄糖挑战（2 g/kg）。用氯异茚明和酚妥拉明进行预处理并没有改变HC引起的高血糖，但确实导致血浆胰岛素水平升高以响应较高的葡萄糖水平。肾上腺切除术并不能阻止 HC 抑制的胰岛素对高血糖的反应。急性剂量的 HC 可能通过中枢激活胰岛交感神经来间接抑制胰岛素释放。
This investigation examined a potential mechanism for the inhibition of insulin release following an acute dose of hydrocortisone sodium succinate (HC). Hydrocortisone (300 mg/kg i.p.) elevated plasma glucose levels (P .ltoreq. 0.05) when administered to male Swiss-Webster mice, without altering plasma insulin levels. This results in a significantly lower insulinogenic index (P .ltoreq. 0.05). Hydrocortisone suppressed the glucose-stimulated insulin levels (P .ltoreq. 0.05) following an i.v. glucose challenge (2 g/kg) in both fed and fasted mice. Pretreatment with chlorisondamine and phentolamine did not alter the HC-induced hyperglycemia but did result in higher plasma insulin levels in response to the higher glucose levels. Adrenalectomy did not prevent the HC-depressed insulin response to hyperglycemia. An acute dose of HC may indirectly suppress insulin release by central activation of the sympathetic nerves at the pancreatic islets.