The Effects of Experimental Hepatobiliary Disease on Certain Aspects of Tocopherol Metabolism in the Rat1

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Abstract
Well nourished rats showed (a) a transient rise in serum tocopherol concentration following acute CCL4-induced hepatic injury, biliary obstruction or external biliary drainage, (b) a decrease in the absorption of tocopherol from the intestinal tract following obstruction or external drainage of the bile duct, but not following acute or chronic CCl4-induced hepatic injury and (c) a significantly greater increase in serum tocopherol following an intramuscular injection of tocopheryl acetate in animals with biliary obstruction, bile fistula or acute hepatic injury than in normal controls, a phenomenon not related to suppression of tocopherol excretion in the bile, but possibly correlated, in part at least, with the retention of serum cholesterols in animals with biliary obstruction. These observations suggest that (a) acute hepatic injury secondary to CC14 administration, ligation of the bile duct or creation of a bile fistula leads to a release of tocopherol stored in the liver, and a reduction in the hepatic uptake of tocopherol from the serum, (b) complete interruption or diversion of bile flow interferes with the absorption of tocopherol from the intestinal tract, (c) hepatocellular injury per se does not affect the serum concentration, absorption or tissue uptake of tocopherol, and (d) the factors leading to hypercholesteremia in obstructive jaundice may play a role in the retention of tocopherol in the serum.