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Foodborne cereulide causes beta-cell dysfunction and apoptosis.

Roman Vangoitsenhoven1, Dieter Rondas1, Inne Crèvecoeur1

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Cereulide, a food toxin, causes beta-cell death and impairs insulin secretion even at low concentrations. Mitochondrial dysfunction is the key mechanism behind these harmful effects on pancreatic beta-cells.

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Area of Science:

  • Endocrinology
  • Toxicology
  • Cell Biology

Background:

  • Cereulide is a toxin found in food, often at low levels.
  • Its effects on pancreatic beta-cells, crucial for insulin production, are not fully understood.

Purpose of the Study:

  • To investigate the impact of cereulide on beta-cell survival and function.
  • To elucidate the mechanisms of cereulide-induced beta-cell toxicity.

Main Methods:

  • Exposure of mouse (MIN6) and rat (INS-1E) beta-cell lines, and mouse islets to varying concentrations of cereulide.
  • Quantification of cell death, assessment of glucose-stimulated insulin secretion (GSIS).
  • Analysis of mitochondrial function, gene expression (mRNA profiling), and ultrastructure (electron microscopy).

Main Results:

  • Low cereulide concentrations (0.5 ng/ml) induced apoptosis in beta-cells and islets, while control cells remained unaffected.
  • GSIS capacity was significantly reduced (P<0.05) after 24h exposure to 0.5 ng/ml cereulide.
  • Mitochondrial dysfunction, including reduced respiration and increased reactive oxygen species, was observed, alongside upregulation of pro-apoptotic markers (Puma, Chop).

Conclusions:

  • Cereulide induces beta-cell apoptosis and impairs function at low concentrations.
  • Mitochondrial dysfunction is a primary mechanism driving cereulide toxicity in beta-cells.
  • Even sub-systemic exposure levels of cereulide are detrimental to pancreatic beta-cells.