Alcohol And the Gastrointestinal Tract: Special Issue: by M. V. Singer, D. Brenner

By M. V. Singer, D. Brenner

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Moreover, in vivo salivary acetaldehyde levels correlate very significantly with the levels that are produced in vitro. This offers the opportunity to use the in vitro salivary test as a tool to investigate possible variables which might influence salivary acetaldehyde production. Salivary acetaldehyde levels after ethanol intake strikingly exceed those known to be derived from endogenous metabolism of ethanol [85]. Via normal distribution and evaporation, salivary acetaldehyde may reach all target tissues of the upper aerodigestive tract.

78 Apte MV, Wilson JS, Korsten MA, McCaughan GW, Haber PS, Pirola RC: Effects of ethanol and protein deficiency on pancreatic digestive and lysosomal enzymes. Gut 1995; 36: 287– 293. 79 Apte M, Norton I, Haber P, Applegate T, Korsten M, McCaughan G, Pirola R, Wilson J: The effect of ethanol on pancreatic enzymes – a dietary artefact? Biochim Biophys Acta 1998; 1379:314–324. 80 Tanaka T, Miura Y, Matsugu Y, Ichiba Y, Ito H, Dohi K: Pancreatic duct obstruction is an aggravating factor in the canine model of chronic alcoholic pancreatitis.

Taken together, these exemplary studies demonstrate the significance of knockout mouse models in alcohol research. Siegmund /Haas /Singer Conclusions and Future Research Animal models are an invaluable tool in gastrointestinal alcohol research. The findings in animal models reveal that ethanol consumption dose-dependently generates epithelial damage in the upper gastrointestinal tract, thus contributing to esophageal dysfunction and gastroesophageal reflux disease, and that ethanol acutely and dosedependently increases gut permeability for endotoxin triggering liver damage.

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