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首页> 外文期刊>Regulatory peptides. >Somatostatin inhibits insulin release via SSTR2 in hamster clonal beta-cells and pancreatic islets.
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Somatostatin inhibits insulin release via SSTR2 in hamster clonal beta-cells and pancreatic islets.

机译:生长抑素通过仓鼠克隆的β细胞和胰岛中的SSTR2抑制胰岛素释放。

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摘要

Somatostatin (SST) inhibits pancreatic endocrine secretion. It is generally accepted that SSTR2 and SSTR5 mediate the inhibition of glucagon and insulin release, respectively. The present study was performed to test the hypothesis that SSTR2, but not SSTR5, mediates SST-induced inhibition of insulin release in hamster beta-cells. Both hamster clonal beta-cells HIT-T15 and pancreatic islets were used to test this hypothesis. Both SST and a nonpeptide SSTR2 agonist L-779,976 (1-100 nM) inhibited insulin release from HIT-T15 and islets in a concentration-dependent manner. In contrast, nonpeptide agonists for SSTR1, 3, 4 and 5 at the highest concentration studied (1 muM) failed to inhibit insulin release. PRL-2903, a peptide SSTR2 antagonist (0.1-1 muM), antagonized SST-induced inhibition of insulin release in a concentration-dependent manner. Taken together, we conclude that, in hamster beta-cells, SST inhibits insulin release via SSTR2 but not SSTR5.
机译:生长抑素(SST)抑制胰腺内分泌。通常接受的是,SSTR2和SSTR5分别介导胰高血糖素和胰岛素释放的抑制。进行本研究以检验以下假设:SSTR2而非SSTR5介导SST诱导的仓鼠β细胞中胰岛素释放的抑制。仓鼠克隆β细胞HIT-T15和胰岛均用于检验这一假设。 SST和非肽SSTR2激动剂L-779,976(1-100 nM)均以浓度依赖的方式抑制胰岛素从HIT-T15和胰岛的释放。相反,在研究的最高浓度(1μM)下,SSTR1、3、4和5的非肽激动剂未能抑制胰岛素释放。 PRL-2903,一种肽SSTR2拮抗剂(0.1-1μM),以浓度依赖性方式拮抗SST诱导的胰岛素释放抑制。两者合计,我们得出的结论是,在仓鼠β细胞中,SST通过SSTR2抑制胰岛素释放,但通过SSTR5抑制胰岛素释放。

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