Regulation of in vitro insulin release from a transplantable syrian hamster insulinoma

Shelley Shapiro, Sumiya Eto, Norman Fleischer, Stephen G. Baum

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

An insulin-producing islet cell tumor of the Syrian hamster has been studied in vitro for its capacity to respond to known stimuli of insulin release. Insulin secretion during short term incubation and perifusion of fragments of tumor was detected by radioimmunoassay. Insulin release was increased 2-4-fold by 40 mM potassium in the presence of calcium, glucose (22 mM), glucagon (0.3- 3.0 μM), N6O2,-dibutyryl adenosine 3′, 5′-monophosphate (cAMP; 6 mM), and theophylline (10 mM). Concentrations of glucagon that induced insulin release were also effective in activating adenylate cyclase in the membranes of tumor cells. Thus, this tumor appears to possess a cAMP-mediated mechanism for insulin release. Somatostatin (0.8-25 μm) inhibited glucagon-induced insulin release without altering basal or glucagon stimulated adenylate cyclase activity. It would appear that inhibition of glucagon induced insulin release by somatostatin is not mediated by adenylate cyclase. We propose that insulin release by this tumor is sufficiently similar to that found in normal islets so as to make it a suitable model for biochemical studies that require large quantities of homogeneous tissue.

Original languageEnglish (US)
Pages (from-to)442-447
Number of pages6
JournalEndocrinology
Volume97
Issue number2
DOIs
StatePublished - Aug 1975

ASJC Scopus subject areas

  • Endocrinology

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