Abstract
ADMINISTRATION of vitamin A to animals decreases the size of the thyroid gland (1–3), lowers oxygen consumption (1–4), and partially cancels the hypermetabolic or lethal effects of exogenous thyroxine or desiccated thyroid (1, 5, 6). These findings suggest that in animals excesses of this vitamin may alter thyroid function or interfere with the peripheral effects of thyroxine and related hormones. Several clinical reports of hyperthyroidism responsive to vitamin A or high fat diet are in keeping with both of these possibilities (7–11). Studies of the possible effects of increased vitamin A intake upon serum protein-bound iodine levels, and upon the disposal of exogenous thyroxine have therefore been undertaken in rats and in man. These indicate that, with sufficient dosage, serum protein-bound iodine concentrations do decrease but that there is no consistent effect upon the disposal of exogenous thyroxine.
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