生长抑素通过SSTR2抑制仓鼠克隆β细胞和胰岛中的胰岛素释放。

Somatostatin inhibits insulin release via SSTR2 in hamster clonal beta-cells and pancreatic islets.

作者信息

Yao Cheng-Yu, Gill Manmeet, Martens Catherine A, Coy David H, Hsu Walter H

机构信息

Department of Biomedical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA, USA.

出版信息

Regul Pept. 2005 Jul 15;129(1-3):79-84. doi: 10.1016/j.regpep.2005.01.012.

DOI:10.1016/j.regpep.2005.01.012

PMID:15927701

Abstract

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 microM) failed to inhibit insulin release. PRL-2903, a peptide SSTR2 antagonist (0.1-1 muicroM), 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.

摘要

生长抑素（SST）抑制胰腺内分泌分泌。一般认为，SSTR2和SSTR5分别介导对胰高血糖素和胰岛素释放的抑制作用。本研究旨在验证以下假说：在仓鼠β细胞中，是SSTR2而非SSTR5介导SST诱导的胰岛素释放抑制作用。采用仓鼠克隆β细胞HIT-T15和胰岛来验证这一假说。SST和非肽类SSTR2激动剂L-779,976（1 - 100 nM）均以浓度依赖方式抑制HIT-T15和胰岛的胰岛素释放。相比之下，在研究的最高浓度（1 μM）下，SSTR1、3、4和5的非肽类激动剂未能抑制胰岛素释放。肽类SSTR2拮抗剂PRL-2903（0.1 - 1 μM）以浓度依赖方式拮抗SST诱导的胰岛素释放抑制作用。综上所述，我们得出结论：在仓鼠β细胞中，SST通过SSTR2而非SSTR5抑制胰岛素释放。