Liver lipid disposal following t-butanol administration to rats

Oral administration of a single dose of t-butanol (25 mmol/kg body wt.) to female Wistar rats results in an accumulation of triacylglycerols (TAGs) in the liver. This administration induces an early increase in the rate of palmitate uptake by the liver and a delayed enhancement of the blood free fatty acid (FFA) level. Whereas hepatic lactate/pyruvate ratio and liver fatty acid oxidation appear unimpaired, a highly significant enhancement of palmitate incorporation into liver TAGs occurs after t-butanol administration. This administration impairs the biosynthesis and/or secretion of very low density lipoproteins (VLDLs) as shown by the decrease in both the serum TAG level and the palmitate incorporation into serum TAGs. These data suggest that the metabolic disturbances reported may be related to the stress induced by the administration of t-butanol which is very slowly metabolized, as shown by the sustained blood alcohol level found over a 20-h period. This study also provides evidence that metabolism through the alcohol dehydrogenase (ADH) pathway is not a prerequisite for the ability of an alcohol to induce a fatty liver when administered to rats.