Relationship between Free Fatty Acid Turnover and Total Body Oxygen Consumption in the Euthyroid and Hyperthyroid States.

Many of the signs and symptoms characteristic of the hyperthyroid state can be elicited in closely similar form by the administration of epinephrine or norepinephrine. Both in clinical and in experimental hyperthyroidism, some receptor systems are known to be more sensitive to catecholamines than they are in the euthyroid state (1). It has been frequently suggested, therefore, that the manifestations of hyperthyroidism are to some extent indirect effects, secondary to enhancement of effective sympathetic activity, rather than direct effects of the thyroid hormone itself. There is convincing evidence that at least some of the cardiovascular manifestations of hyperthyroidism are indeed due to enhanced sympathetic activity (2, 3). However, the evidence with regard to the hypermetabolism of the hyperthyroid state is more difficult to evaluate. Some studies have shown a partial correction toward normal by chemical or surgical interference with the activity of the sympathetic system (2, 4-6), whereas other similar studies have shown no such effect (7, 8). We have reported previously that the calorigenic effect of intravenously infused norepinephrine can be prevented by prior administration of a /8-adrenergic blocking agent, pronethalol (9). These studies also showed that norepinephrineinduced fat mobilization was blocked, suggesting a relationship between free fatty acid mobilization and calorigenesis. Because chronic toxicity experiments in rats subsequently showed that pronethalol might have carcinogenic potential, use of this effective blocking agent in man was abandoned in continuing studies. However, Carlson and Or6 (10) have shown that intravenously administered nicotinic acid is also capable of blocking catecholamine-induced FFA mobilization. In