The thyroid hormones act directly on mitochondria, and thereby control the transformation of the energy derived from oxidations into a form utilizable by the cell. Through their direct actions on mitochondria, the hormones also control indirectly the rate of protein synthesis and thereby the amount of oxidative apparatus in the cell. A rationale for the effects of thyroid hormone excess or deficiency is based upon studies of the mechanism of thyroid hormone action. In hypothyroidism, slow fuel consumption leads to a low output of utilizable energy. In hyperthyroidism, rapid fuel consumption leads to a high energy output, but as efficiency decreases, the utilizable energy produced decreases. Many of the chemical and physical features of these diseases can be reduced to changes in available energy.
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↵* Abbreviations: L-T4, L-thyroxine; L-T3, L-triiodothyronine; Triac, triiodothyroacetic acid; ATP, ADP and AMP, adenosine tri-, di- and mono-phosphate; P1, inorganic phosphate; NADH and NADPH, reduced nicotinamideadenine dinucleotide and dinucleotide phosphate; DNP, 2,4-dinitrophenol; BMR, basal metabolic rate (O2 consumption).
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