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ShareJune 9, 2008 — Much is known about the mechanisms by which excessive alcohol consumption causes damage to organs such as the liver, heart, and brain.
However, only recently has progress been made in understanding how excessive alcohol consumption causes damage to the pancreas, and new insight into the molecular mechanisms underlying pancreatic damage in mice following alcohol exposure has now been provided by Herbert Gaisano and colleagues at the University of Toronto and University Health Network, Canada.
Rodents who have been fed alcohol in their diet and then exposed to a drug known as carbachol develop an inflammation of the pancreas (pancreatitis) that resembles the pancreatitis seen in individuals who consume an excessive amount of alcohol.
It has been suggested previously that the rodents develop pancreatitis because the alcohol and carbachol exposure cause cells in the pancreas to release vesicles containing degradative proteins known as enzymes at inappropriate places.
In the study, a protein known as VAMP8 was found to have an important role in coordinating the inappropriate release of enzyme-containing vesicles in mice exposed to alcohol and carbachol. As such, mice lacking VAMP8 showed reduced pancreatitis after exposure to alcohol and carbachol.
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The above story is reprinted from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.
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Journal Reference:
- VAMP8 is the v-SNARE that mediates basolateral exocytosis in a mouse model of alcoholic pancreatitis. Journal of Clinical Investigation, June 5, 2008
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