Palmitate induced lipoapoptosis of exocrine pancreas AR42J cells |
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Authors: | Z Landau E Forti M Alcaly R Z Birk |
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Institution: | (1) Ben-Gurion University of the Negev, Beer-Sheva, 84105, Israel |
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Abstract: | Chronic surplus of dietary consumption, typical to obesity, results in overflow of fat to non-adipose tissues. Intracellular
accumulation of fat in non-adipose tissues is associated with cellular dysfunction and cell death and ultimately contributes
to the pathogenesis of chronic diseases. The influence of fat overflow on the exocrine pancreas is not known. The purpose
of this research was to study the lipotoxic and lipoapoptotic effect of prolonged (72 h) long chain saturated palmitic fatty
acid (0.1 mM) on the survival of exocrine pancreas AR42J cells. We demonstrate that chronic exposure of AR42J cells to palmitic
acid results in significant increase in triglycerides accumulation (up to 25% of cells area), compared to untreated cultures.
Lipid accumulation prompted a typical apoptotic process, demonstrated by both DNA fragmentation and condensed chromatin appearance
(DAPI staining). Quantitative real-time PCR studies demonstrated that prolonged palmitic acid supplementation induced down-regulation
of the anti-apoptotic Bcl2 mRNA levels (22%) and up-regulation of the pro-apoptotic Bax mRNA levels (300%), leading to disruption
of the pro/anti apoptotic balance (Bax/Bcl2=3). No major change was detected in iNOS mRNA expression.
In conclusion, prolonged exposure to saturated palmitic acid induces lipoapoptosis in exocrine pancreatic AR42J cells, through
disturbance of the Bax/Bcl-2 balance. |
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Keywords: | apoptosis AR42J exocrine pancreas palmitic acid |
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