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Ethanol induced acinar cell injury

M V Apte1, I D Norton, J S Wilson

  • 1Department of Gastroenterology, Prince of Wales Hospital, Sydney, Australia.

Alcohol and Alcoholism (Oxford, Oxfordshire). Supplement
|January 1, 1994
PubMed
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Ethanol abuse primes the pancreas for autodigestion by increasing digestive enzymes and lysosomal enzyme cathepsin B. This research identifies cellular changes in the "Drinker's Pancreas" but not the specific triggers for pancreatitis.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Toxicology

Background:

  • Alcohol abuse is a significant risk factor for pancreatitis.
  • Previous research has not identified predisposing factors in alcoholics.
  • Ethanol's metabolic effects on pancreatic acinar cells are under investigation.

Purpose of the Study:

  • To investigate the metabolic effects of ethanol on pancreatic acinar cells.
  • To understand how ethanol may predispose the pancreas to autodigestion.

Main Methods:

  • Utilized the Lieber-DeCarli model of ethanol administration in rats.
  • Examined changes in pancreatic acinar cells associated with ethanol exposure.

Main Results:

  • Ethanol increased pancreatic digestive enzyme content via elevated mRNA levels.

Related Experiment Videos

  • Glandular cathepsin B, a trypsinogen activator, was also increased.
  • Lysosomes and zymogen granules showed increased fragility, potentially due to cholesteryl and fatty acid ethyl esters.
  • These changes create a "primed" state in the pancreas, termed the "Drinker's Pancreas".

    • Conclusions:

    • Ethanol induces significant cellular changes in the pancreas, predisposing it to autodigestion.
    • The identified cellular alterations include increased enzyme content and lysosomal/zymogen granule fragility.
    • Specific triggering factors for autodigestion in this ethanol-induced state remain unidentified.