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胰高血糖素介导精氨酸诱导的离体大鼠胰岛分泌生长抑素。

Glucagon mediates arginine-induced somatostatin secretion from isolated rat pancreatic islets.

作者信息

Vonen B, Florholmen J, Malm D, Torjessen P, Burhol P G

机构信息

Department of Medicine, University Hospital of Tromsø, Norway.

出版信息

Scand J Clin Lab Invest. 1992 Apr;52(2):107-12. doi: 10.3109/00365519209088773.

Abstract

Glucagon has been suggested to be a mediator of intra-islet paracrine effect of insulin and somatostatin during nutritive stimulation. The aim of this study was to reveal possible intra-islet interactions between insulin, somatostatin and glucagon in a batch stimulation model with isolated pancreatic islets. Such interactions may influence stimulus-secretion experiments in this experimental model. In our hands arginine stimulated somatostatin secretion only in the presence of insulin antiserum. Furthermore, arginine-induced glucagon secretion was greatly increased following addition of insulin antiserum. The addition of glucagon antiserum inhibited these effects of insulin antiserum on somatostatin secretion. In conclusion, glucagon apparently represents the central mediator of arginine effects on somatostatin secretion in isolated rat pancreatic islets in batch stimulation experiments.

摘要

胰高血糖素被认为是营养刺激期间胰岛内胰岛素和生长抑素旁分泌作用的介质。本研究的目的是在分离的胰岛批量刺激模型中揭示胰岛素、生长抑素和胰高血糖素之间可能存在的胰岛内相互作用。这种相互作用可能会影响该实验模型中的刺激-分泌实验。在我们的实验中,精氨酸仅在存在胰岛素抗血清的情况下刺激生长抑素分泌。此外,添加胰岛素抗血清后,精氨酸诱导的胰高血糖素分泌大大增加。添加胰高血糖素抗血清可抑制胰岛素抗血清对生长抑素分泌的这些作用。总之,在批量刺激实验中,胰高血糖素显然是精氨酸对分离的大鼠胰岛生长抑素分泌作用的中心介质。

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