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Calcium affects insulin release and membrane potential in islet beta-cells
The American Journal of Physiology
|January 1, 1981
Summary
Calcium and magnesium concentrations, along with beta-cell membrane potential, significantly influence insulin release. Altering these factors can modulate glucose-stimulated insulin secretion, revealing complex regulatory mechanisms.
Area of Science:
- Endocrinology
- Cell Physiology
- Pancreatic Beta-Cell Function
Background:
- Insulin secretion is a complex process regulated by various ions and cellular electrical activity.
- The roles of calcium (Ca) and magnesium (Mg) in glucose-stimulated insulin release (GSIR) and their interplay with membrane potential require further elucidation.
Purpose of the Study:
- To investigate the relationship between insulin release and beta-cell membrane potential under varying Ca and Mg concentrations.
- To determine how alterations in Ca and Mg levels affect GSIR and cellular electrical activity.
Main Methods:
- Perfusion of rat pancreas and perifusion of mouse islets to measure insulin release.
- Electrophysiological recordings of single beta-cell membrane potentials.
- Manipulation of extracellular Ca and Mg concentrations during glucose stimulation.
Main Results:
- Beta-cell depolarization correlated with insulin release, while hyperpolarization suppressed it, independent of Ca concentration.
- Reduced Ca and Mg maintained GSIR with sustained depolarization and altered burst activity patterns.
- Re-addition of Ca and Mg transiently suppressed insulin release, linked to hyperpolarization, primarily due to Ca.
Conclusions:
- Relative Ca and Mg concentrations and membrane potential are critical determinants of insulin release.
- Under specific conditions, Ca can inhibit GSIR, potentially by enhancing potassium permeability.