Somatostatin inhibits insulin release via SSTR2 in the hamster pancreatic islets

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2004-01-01
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Yao, Cheng-Yu
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Animal Science

The Department of Animal Science originally concerned itself with teaching the selection, breeding, feeding and care of livestock. Today it continues this study of the symbiotic relationship between animals and humans, with practical focuses on agribusiness, science, and animal management.

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The Department of Animal Husbandry was established in 1898. The name of the department was changed to the Department of Animal Science in 1962. The Department of Poultry Science was merged into the department in 1971.

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It is generally accepted that somatostatin receptor subtype 5 (SSTR5) mediates the inhibition of insulin release. This is due to the fact that in the human, rat, and mouse somatostatin (SST) inhibits insulin release via SSTR5; however, in a preliminary study from Dr. Hsu's laboratory with HIT-T15 [beta]-cells that are derived from hamster insulinoma, it was found that a SSTR2 agonist, but not other SSTR agonists, inhibited insulin release. Since SSTR2 is highly expressed in tumor cells, it is possible that the results from HIT-T15 cells may be due to the nature of tumor cells. Thus, it is hypothesized that in hamsters, SSTR2 mediates somatostatin-induced inhibition of insulin release. Isolated hamster pancreatic islets were used in the present study to test this hypothesis. Both somatostatin (1-100 nM) and nonpeptide SSTR2 agonist L-779,976 (0.1-100 nM) inhibited insulin release in a dose-dependent manner. Nonpeptide agonists for SSTR1, 3, 4, and 5 at the highest concentration studied (1[mu]M) failed to inhibit insulin release. PRL-2903, a peptide SSTR2 antagonist (0.3-1[mu]M), antagonized somatostatin-induced inhibition of insulin release in a dose-dependent manner. It is concluded that in hamster [beta]-cells, somatostatin inhibits insulin release via SSTR2 but not SSTR5.

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Thu Jan 01 00:00:00 UTC 2004