Thyrotoxicosis as a Disease of Mitochondria

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Abstract
THE physiologic manifestations of the cellular action of the thyroid hormones are documented extensively. The high basal metabolic rate of the hyperthyroid mammal1 is accompanied by an increased rate of oxidation in most of the tissues2; this suggested, as early as 1927, that thyroxine is a necessary component, or coenzyme, of oxidative enzymes.3 A review of investigations up to 1951 based upon such a hypothesis, however, does not define an enzyme or system of enzymes requiring thyroxine for action.4 Biochemical investigations since that time demonstrate that thyroid hormones produce functional changes in oxidative phosphorylation and structural changes in mitochondria. . . .