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血清素诱导小鼠出现低血糖及血清胰岛素水平升高。

Serotonin-induced hypoglycemia and increased serum insulin levels in mice.

作者信息

Yamada J, Sugimoto Y, Kimura I, Takeuchi N, Horisaka K

机构信息

Department of Pharmacology, Kobe Women's College of Pharmacy, Japan.

出版信息

Life Sci. 1989;45(20):1931-6. doi: 10.1016/0024-3205(89)90547-x.

Abstract

The effects of serotonin (5-HT) on plasma glucose levels were studied. 5-HT above 20 mg/kg induced apparent hypoglycemia in mice. The hypoglycemic effects of 5-HT were strongly antagonized by methysergide but only partially inhibited by ketanserin. However, ICS 205-930 was without effect. This indicates that the hypoglycemia induced by 5-HT is mediated by both the 5-HT1 and 5-HT2 receptors. 5-HT also produced an increase in serum immunoreactive insulin (IRI) which was completely inhibited by methysergide and partially antagonized by ketanserin. It is suggested that the 5-HT-induced increase in IRI is elicited by the activation of the 5-HT1 and 5-HT2 receptors, which is similar to the results obtained with plasma glucose. These results indicate that the 5-HT receptors may regulate blood glucose levels by modifying the release of insulin.

摘要

研究了血清素(5-羟色胺,5-HT)对血浆葡萄糖水平的影响。20毫克/千克以上的5-HT可使小鼠出现明显的低血糖。麦角酰二乙胺能强烈拮抗5-HT的降血糖作用,而酮色林只能部分抑制该作用。然而,ICS 205-930则无此作用。这表明5-HT诱导的低血糖是由5-HT1和5-HT2受体介导的。5-HT还使血清免疫反应性胰岛素(IRI)增加,这一作用被麦角酰二乙胺完全抑制,被酮色林部分拮抗。提示5-HT诱导的IRI增加是由5-HT1和5-HT2受体的激活引起的,这与血浆葡萄糖的实验结果相似。这些结果表明,5-HT受体可能通过调节胰岛素的释放来调控血糖水平。

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