Propylthiouracil, Thyroid, and Dietary Liver Injury

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Abstract
The effect of propylthiouracil in retarding the appearance of dietary (low choline) cirrhosis is partly due to the reduced caloric intake of rats given the drug. Restricting the food intake of control rats to the same degree also delayed the appearance of cirrhosis. The thyroid hormone influences the site and manner of deposition of fat in the liver lobule. Fat tends to be laid down throughout the lobule as intracellular lipid in the livers of rats with deficient thyroid function. With normal thyroid function, or especially if thyroid is fed to rats, lipid tends to accumulate in the central part of the lobule, and even when the level of fat in the liver is low, extracellular fatty cysts are frequently formed. The etiological relationship of extracellular deposition of fat to the production of dietary cirrhosis is discussed. It is suggested that in addition to its effect on caloric intake, propylthiouracil also exerts a more direct effect in retarding the development of cirrhosis, by preventing the synthesis of thyroid hormone and thus influencing the manner of deposition of fat in the liver.