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.
","abstract_html":"<p>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.</p>","abstract_has_math":false,"creators":["Yao, Cheng-Yu"],"institution":null,"degree_name":"Master of Science","degree_level":"thesis","degree_discipline":"Animal Physiology","degree_department":"Department of Animal Science","school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2004,"date_issued":"2004-01-01","date_published":"2004-01-01","updated_at":"2026-07-24T02:38:23Z","subjects":[],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.31274/rtd-180813-8302"],"render_values":[{"text":"https://doi.org/10.31274/rtd-180813-8302","href":"https://doi.org/10.31274/rtd-180813-8302","code":true}]},{"key":"dc:identifier","label":"Identifier","values":["archive/lib.dr.iastate.edu/rtd/17520/"],"render_values":[{"text":"archive/lib.dr.iastate.edu/rtd/17520/","href":null,"code":true}]}]},"links":{"outbound_url":"https://dr.lib.iastate.edu/handle/20.500.12876/71343","outbound_label":"Repository record","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.department","label":"Department","values":["Department of Animal Science"]},{"key":"dc:creator","label":"Author","values":["Yao, Cheng-Yu"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2018-08-22T17:07:53.000"]},{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2020-06-30T08:00:37Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2020-06-30T08:00:37Z"]},{"key":"dc:date.issued","label":"Date","values":["2004-01-01"]},{"key":"dc:type","label":"Dc Type","values":["thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Animal Physiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["archive/lib.dr.iastate.edu/rtd/17520/"]},{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.31274/rtd-180813-8302"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://dr.lib.iastate.edu/handle/20.500.12876/71343"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["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.
"]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Somatostatin inhibits insulin release via SSTR2 in the hamster pancreatic islets"]}]}],"canonical_facts":{"dc:contributor.department":["Department of Animal Science"],"dc:creator":["Yao, Cheng-Yu"],"dc:date":["2018-08-22T17:07:53.000"],"dc:date.accessioned":["2020-06-30T08:00:37Z"],"dc:date.available":["2020-06-30T08:00:37Z"],"dc:date.issued":["2004-01-01"],"dc:description.abstract":["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.
"],"dc:format.mimetype":["application/pdf"],"dc:identifier":["archive/lib.dr.iastate.edu/rtd/17520/"],"dc:identifier.doi":["https://doi.org/10.31274/rtd-180813-8302"],"dc:identifier.uri":["https://dr.lib.iastate.edu/handle/20.500.12876/71343"],"dc:language.iso":["en"],"dc:title":["Somatostatin inhibits insulin release via SSTR2 in the hamster pancreatic islets"],"dc:type":["thesis"],"thesis:degree_discipline":["Animal Physiology"],"thesis:degree_level":["thesis"],"thesis:degree_name":["Master of Science"]},"updated_at":"2026-07-24T02:38:23Z"}