Related Experiment Videos
Calcium-antagonists and islet function. VI. Effects of barium
Pflugers Archiv : European Journal of Physiology
|September 3, 1976
Summary
Barium (Ba2+) triggers insulin release from pancreatic B-cells by accumulating within them. This process involves specific ion channels and is modulated by various substances, suggesting a key role for divalent cation accumulation.
Area of Science:
- Endocrinology
- Cell Biology
- Pharmacology
Background:
- Insulin secretion is crucial for glucose homeostasis.
- Divalent cations play a significant role in regulating insulin release.
- The specific mechanisms of barium (Ba2+)-induced insulin release require further elucidation.
Purpose of the Study:
- To investigate the mechanism of Ba2+-induced insulin release in isolated perfused rat pancreas.
- To determine the influence of other ions and substances on Ba2+ uptake and insulin secretion.
- To elucidate the role of B-cell cation accumulation in triggering insulin release.
Main Methods:
- Utilized an isolated perfused rat pancreas model.
- Measured 133Ba2+ net uptake in isolated pancreatic islets.
- Investigated the effects of calcium (Ca2+), magnesium (Mg2+), verapamil, EGTA, theophylline, glucose, and cytochalasin B on Ba2+ uptake and insulin release.
Main Results:
- Ba2+-induced insulin release was inhibited by Ca2+, Mg2+, and verapamil, but enhanced by EGTA, theophylline, glucose, and cytochalasin B.
- Ca2+, Mg2+, and verapamil inhibited 133Ba2+ net uptake into islets.
- Glucose enhanced 133Ba2+ uptake only after sufficient Ba2+ accumulation; theophylline did not affect uptake but enhanced release.
Conclusions:
- Ba2+-induced insulin release depends on its accumulation within pancreatic B-cells.
- Ba2+ transport into B-cells occurs via a verapamil-sensitive channel with competitive interactions from Ca2+ and Mg2+.
- Theophylline may enhance insulin release through intracellular cation translocation, supporting the role of critical divalent cation accumulation in triggering insulin release.