Foodborne Cereulide Causes Beta-Cell Dysfunction and ApoptosisReportar como inadecuado

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To study the effects of cereulide, a food toxin often found at low concentrations in take-away meals, on beta-cell survival and function.


Cell death was quantified by Hoechst-Propidium Iodide in mouse MIN6 and rat INS-1E beta-cell lines, whole mouse islets and control cell lines HepG2 and COS-1. Beta-cell function was studied by glucose-stimulated insulin secretion GSIS. Mechanisms of toxicity were evaluated in MIN6 cells by mRNA profiling, electron microscopy and mitochondrial function tests.


24 h exposure to 5 ng-ml cereulide rendered almost all MIN6, INS-1E and pancreatic islets apoptotic, whereas cell death did not increase in the control cell lines. In MIN6 cells and murine islets, GSIS capacity was lost following 24 h exposure to 0.5 ng-ml cereulide P<0.05. Cereulide exposure induced markers of mitochondrial stress including Puma p53 up-regulated modulator of apoptosis, P<0.05 and general pro-apoptotic signals as Chop CCAAT-enhancer-binding protein homologous protein. Mitochondria appeared swollen upon transmission electron microscopy, basal respiration rate was reduced by 52% P<0.05 and reactive oxygen species increased by more than twofold P<0.05 following 24 h exposure to 0.25 and 0.50 ng-ml cereulide, respectively.


Cereulide causes apoptotic beta-cell death at low concentrations and impairs beta-cell function at even lower concentrations, with mitochondrial dysfunction underlying these defects. Thus, exposure to cereulide even at concentrations too low to cause systemic effects appears deleterious to the beta-cell.

Autor: Roman Vangoitsenhoven, Dieter Rondas, Inne Crèvecoeur, Wannes D-Hertog, Pieter Baatsen, Matilde Masini, Mirjana Andjelkovic, Jor



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