Does chronic ethanol intake cause chronic pancreatitis?: evidence and mechanism.
Λέξεις-κλειδιά
Αφηρημένη
OBJECTIVE
To demonstrate the relationship between prolonged alcohol intake and chronic pancreatitis.
METHODS
Wistar rats were fed diet containing 25% concentration (vol/vol) of ethanol for 6 months. Cholecystokinin (CCK) was quantified by radioimmunoassay. Immunohistochemistry was used to detect alpha-smooth muscle actin, cyclooxygenase 2, and toll-like receptor 4 in rat pancreas. Western-blot was used to quantitatively determine the expression of nuclear factor kappaB and the above inflammatory markers. Pancreatic collagen content was quantified by measuring OH-proline. Superoxide dismutase was measured by colorimetric method.
RESULTS
In contrast to the control group, there was little histological change in pancreatic tissue but obvious ultrastructural changes in acinar cells of the ethanol group. Cholecystokinin, amylase, and lipase were found reduced in the ethanol group. Chronic ethanol intake did not elicit any change in the expression of alpha-smooth muscle actin, cyclooxygenase 2, toll-like receptor 4, nuclear factor kappaB, pancreatic collagen, and superoxide dismutase.
CONCLUSIONS
Long-term alcohol consumption did not cause chronic pancreatitis but impaired exocrine pancreatic function. The mechanism behind it could be associated with decreased output of intestinal CCK and lower concentration of pancreatic CCK. Furthermore, the nonoxidative pathway of ethanol metabolism was probably involved in it.
