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Ascorbic acid and insulin secretion in pancreatic islets

P Bergsten1, A S Moura, I Atwater

  • 1Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.

The Journal of Biological Chemistry
|January 14, 1994
PubMed
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Ascorbic acid (vitamin C) rapidly inhibits glucose-stimulated insulin secretion from pancreatic islets in a dose-dependent manner. This effect, linked to beta-cell hyperpolarization, may explain why vitamin C levels are tightly regulated in the body.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Biochemistry

Background:

  • Insulin secretion is crucial for glucose homeostasis.
  • Ascorbic acid (vitamin C) plays various biological roles, but its direct effect on insulin release is not fully understood.
  • Pancreatic beta-cells are responsible for insulin production and secretion.

Purpose of the Study:

  • To investigate the acute effect of ascorbic acid on glucose-induced insulin release from pancreatic islets.
  • To determine the dose-dependency and reversibility of ascorbic acid's action on insulin secretion.
  • To explore the underlying cellular mechanisms, specifically changes in pancreatic beta-cell membrane potential.

Main Methods:

  • Utilized a novel, ultra-sensitive enzyme-linked immunosorbent insulin assay to measure insulin secretion from single pancreatic islets.

Related Experiment Videos

  • Administered varying concentrations of ascorbic acid to assess dose-dependent effects.
  • Monitored pancreatic beta-cell membrane potential to evaluate changes in electrical activity.
  • Assessed the reversibility of observed effects after ascorbic acid removal.

    • Main Results:

    • Ascorbic acid rapidly inhibited glucose-induced insulin secretion within 20 seconds.
    • The inhibition was dose-dependent, with 200 microM causing 50% inhibition and 400 microM causing 90% inhibition.
    • The inhibitory effect was completely reversible upon removal of ascorbic acid.
    • Ascorbic acid induced hyperpolarization of pancreatic beta-cells, suppressing glucose-induced membrane depolarization.
    • The reduction in insulin secretion correlated with diminished amplitudes of fast insulin release transients.

    Conclusions:

    • Ascorbic acid exerts a potent, rapid, and reversible inhibitory effect on glucose-stimulated insulin secretion.
    • The mechanism involves hyperpolarization of pancreatic beta-cells, suppressing electrical activity.
    • These findings provide a potential explanation for the tight physiological control of plasma ascorbate concentrations.