METABOLIC EFFECTS IN MAN OF THE ACETICACID ANALOGUES OF THYROXINE AND TRIIODOTHYRONINE

Abstract

Triiodothyroacetic acid (3:5-diiodo-4-(3′-iodo-4′-hydroxyphenoxy)-phenyl acetic acid—hereinafter called triac) has been reported to cause, within thirty minutes, an increase in oxygen consumption in rat kidney slices (1). This effect was largely gone within four hours. In rats, triac and tetraiodothyroacetic acid (tetrac) have been tested for their antigoitrogenic properties and their effect on oxygen consumption. In general, both compounds are effective and have about one-tenth the potency of their respective parent compounds (2). It has been further shown that triac can induce changes in the feathers of birds, similar to those induced by thyroid hormone (3). In human subjects, triac has been reported to cause remission in the clinical features of myxedema and a depression in the serum cholesterol level, without change in basal oxygen consumption (4). In another study on a single case of myxedema a rise in basal metabolic rate (BMR) was observed after the administration of triac (5). It has been suggested that, because of its unusually rapid action in vitro, triac may represent the form in which the thyroid hormone exists in the tissues. (1). This is an attractive hypothesis biochemically, since the keto acids of both thyroxine (T4) and triiodothyronine (T3) have been identified, and further oxidation of the next lower acid (in this case, the acetic acid compound) seems a likely reaction (6). Furthermore, the presence of triac in the kidneys of rats given labeled T3 has recently been demonstrated (7).