Metabolic aspects of the calorigenic effect of thyroid hormone in mammals.

The increased BMR in hyperthyroidism may be accounted for by the use of chemical energy for metabolic processes and work. Major contributors are the heart work and futile cycling of FFA into triglyceride in adipose tissue, whereas gluconeogenesis in liver and the maintenance of sodium and potassium concentration gradients across the plasma membranes are unlikely to play any significant role. Information on the use of energy for protein turnover and urea production is lacking. The rate of oxygen uptake is not increased in the brain, spleen and testis. The main metabolic fuel seems to be free fatty acid. The mechanism which enables the hyperthyroid tissue to maintain normal concentrations of ATP, ADP and inorganic phosphate, (Pi) despite an increased turnover of energy-rich phosphates, is not fully elucidated. However, ultimately the increased rate of oxygen uptake in hyperthyroidism seems to rely upon an increased capacity for the transport of cytosolic ADP and Pi into mitochondria. The transport capacity is increased by an increased area of the mitochondrial membrane per g tissue and by a change in the kinetics of translocation of substrates for oxidative phosphorylation. Other transport processes across the mitochondrial membrane are also changed by hyperthyroidism, e.g. long chain fatty acid transport via carnitine acyl transferase, and oxaloacetate transport via substrate shuttles.