Non-oxidative metabolism of ethanol by rat pancreatic acini.
BACKGROUND: The pathogenesis of alcoholic pancreatitis may involve the metabolism of ethanol (via oxidative and non-oxidative pathways) within the pancreas. The aims of this study were to determine the rate of non-oxidative metabolism in isolated rat pancreatic acini and to compare this to the rate of ethanol oxidation. METHODS: Pancreatic acini were isolated from male Sprague-Dawley rats and incubated with (14)C-ethanol. Radiolabelled fatty acid ethyl esters (non-oxidative metabolites) were isolated from lipid extracts by thin-layer chromatography. Radiolabelled acetate (oxidative metabolite) was isolated from the incubation medium by ion-exchange chromatography. RESULTS: Non-oxidative metabolism by isolated pancreatic acini was demonstrated. At 50 and 100 mmol/l ethanol, fatty acid ethyl ester concentrations were 49.6 +/- 13.3 and 199 +/- 93 micromol/l, respectively. These levels have previously been shown to result in tissue injury. Non-oxidative metabolism was increased 9-fold by addition of oleic acid and inhibited by the lipase inhibitor, tetrahydrolipstatin, by 91.05 +/- 1.99%. The rate of oxidative metabolism was 21-fold higher than that of non-oxidative metabolism. CONCLUSIONS: Intact pancreatic cells metabolize ethanol by the non-oxidative pathway, generating fatty acid ethyl esters at a rate sufficient to cause pancreatic damage. Oxidative metabolism of ethanol occurs at a much higher rate and may also play a role in pancreatitis.[1]References
- Non-oxidative metabolism of ethanol by rat pancreatic acini. Haber, P.S., Apte, M.V., Moran, C., Applegate, T.L., Pirola, R.C., Korsten, M.A., McCaughan, G.W., Wilson, J.S. Pancreatology (2004) [Pubmed]
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