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Calcium-antagonists and islet function. V. Effect of R33711
Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|November 1, 1976
Summary
R33711 drug blocks calcium entry into pancreatic beta cells, inhibiting glucose-stimulated insulin release. This calcium channel blocker affects insulin secretion pathways, impacting glucose metabolism.
Area of Science:
- Pharmacology
- Endocrinology
- Cell Biology
Background:
- Insulin secretion is a complex process regulated by various factors, including glucose and calcium ions.
- Calcium influx into pancreatic beta cells is crucial for stimulus-secretion coupling in insulin release.
Purpose of the Study:
- To investigate the effects of R33711, a potential calcium antagonist, on glucose- and sulfonylurea-stimulated insulin release.
- To elucidate the mechanism by which R33711 influences insulin secretion at the cellular level.
Main Methods:
- Utilized isolated pancreatic islets to assess insulin release in response to glucose and gliclazide.
- Measured the uptake of 45Ca2+ by isolated islets in the presence and absence of R33711.
- Assessed glucose-stimulated lactate production and 45Ca2+ efflux rates.
Main Results:
- R33711 suppressed glucose- and gliclazide-stimulated insulin release, but not theophylline-induced release.
- A low concentration (0.2 muM) of R33711 abolished glucose-induced insulin release.
- R33711 inhibited net 45Ca2+ uptake by islets, independent of glucose or sulfonylurea presence.
- R33711 did not affect glucose-stimulated lactate production or calcium efflux dynamics.
Conclusions:
- R33711 acts by inhibiting calcium entry into pancreatic beta cells.
- This calcium influx is essential for the maintenance of the calcium-dependent insulin secretory process.
- R33711 represents a potential therapeutic agent targeting calcium channels involved in insulin regulation.