The Role of Thyroid Activity in the Pathogenesis of Hepatic Lesions Due to Choline and Cystine Deficiency

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Abstract
A decreased level of thyroid activity, induced by thyroidectomy, thiouracil or p-aminobenzoic acid feeding, prevents or retards the development of hepatic necrosis or fibrosis associated with choline and cystine deficiencies. Although thyroid feeding hastened the death of choline-deficient rats, their livers contained little fat and showed no necrosis or fibrosis. Thyroid feeding hastened the death of cystine-deficient rats; their livers exhibited the acute necrosis characteristic of this deficiency. Rats living on a commercial chow were more resistant to the toxic effects of hyperthyroidism than animals on our best synthetic ration. The further addition of choline or methionine to this synthetic diet somewhat increased the susceptibility of rats to thyroid toxicity. Animals on low protein diets were more susceptible to thyroid toxicity than those on high protein diets, and animals on high fat diets were somewhat more resistant than those on low fat diets. Animals deficient in both cystine and choline were more susceptible to hyperthyroidism than any other group studied. The existence of an already established fatty liver appeared to protect the rat against thyrotoxicosis. The inclusion of sulfasuxidine, taurine or inositol in a choline-deficient diet prevented the development of cirrhosis during the experimental period but not by virtue of lipotropic action or antithyroid activity, as judged by liver fat content and the histological appearance of the thyroid.