Summary
The pancreatic tumor cells (In 111) derived from BK virusinduced insulinoma of Syrian
golden hamsters were maintained in culture for several passages and were studied for
their insulin secretory ability under various stimulatory conditions. Insulin release
was not increased by D-glucose stimulation (27.8 mM), while dibutylyl cyclic AMP (1
mM), theophylline (1 mM), 3-isobutyl-I-methylxanthine (0.1 mM) and elevation of medium
calcium from 0.5 to 2.7 mM stimulated insulin release 2.5- to 4-fold. There was a
concomitant increase of medium cyclic AMP with addition of theophylline. Streptozotocin
(2 mM) treatment for 48 hours significantly reduced insulin release, while alloxan
(2 mM), had no inhibitory effect on insulin release. The results indicate that while
in vitromaintained islet tumor cells. In 111, have a cyclic AMP-mediated process involved
in insulin secretion analogous to normal beta cells, these cells lack the ability
to recognize glucose as an insulin secretagogue probably due to a defect in the cell
membrane, though the possibility of alteration in glucose metabolism cannot be fully
excluded.
Key-Words:
Insulinoma Cell
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Insulin Release
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Cyclic AMP
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Alloxan
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Streptozotocin
