Abstract
Summary
Since pyrazole specifically inhibits liver alcohol dehydrogenase and impairs the metabolism of ethanol, studies were undertaken in rats to evaluate the influence of inhibition of ethanol metabolism on the development of an acute ethanol-induced fatty liver. In agreement with previous observations, 20 hr after ethanol administration a 5-fold increase in hepatic triglyceride concentration occurred. In marked contrast, the pyrazole- and ethanol-treated group showed complete inhibition of ethanol-induced hepatic triglyceride accumulation. The prevention of the ethanol-induced hepatic triglyceride accumulation occurred in the presence of enhanced blood ethanol concentrations in the pyrazole group. The carbon tetrachloride-induced fatty liver and plasma hypotrigly-ceridemia was not modified by pyrazole, denoting specificity in the pyrazole inhibition of ethanol-induced hepatic injury. These findings demonstrate that pyrazole can completely prevent the development of the ethanol-induced fatty liver in the presence of elevated concentrations of blood ethanol. Thus, ethanol, per se, is not the causative factor in fatty liver development.
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