EXTRATHYROIDAL ACTIONS OF PITUITARY THYROTROPIN: EFFECTS ON THE CARBOHYDRATE, LIPID AND RESPIRATORY METABOLISM OF RAT ADIPOSE TISSUE

The thesis that pituitary thyrotropin (thyroid-stimulating hormone, TSH) affects multiple facets of intrathyroidal metabolism and that changes in iodine economy may constitute merely one ex-pression of these alterations (1, 2) is supported by many published reports. These are summarized in Table I. Only data derived by the direct ad-dition of TSH to in vitro systems have been tabu-lated since, herein, the possible metabolic adapta-tions to changes in thyroid blood flow need not be considered. The in vitro approach has demonstrated that a variety of the oxidative, assimilative and meta-bolic functions of surviving thyroid tissue are stim-ulated when TSH is introduced into media con-taining serum, or other potential organic sub-strates (3-8) (Table I, A). However, TSH also alters the respiration, hydration, and cytostruc-tural lipids of thyroid tissue even in simple sa-line media (1, 9-12) (Table I, B). The occur-rence of the latter phenomena in the absence of exogenous organic metabolites has prompted the suggestion that TSH primarily initiates a realign-ment of existing intrathyroidal pathways and/or a mobilization of preformed intrathyroidal sub-strates ( 5). In order to find an extrathyroidal counterpart for this postulated sequence, the effects of TSH upon adipose tissue have been examined. The inquiry was stimulated by the suggestions of Engel, Engel and McPherson that the generalized metabolic action of pituitary hormones may mimic their effects upon target glands (13, 14). In th

STUDIES OF THYROID FUNCTION AND THE PERIPHERAL METABOLISM OF Il31-LABELED THYROXINE IN PATIENTS WITH TREATED GRAVES' DISEASE 1 2

Recent studies have revealed an abnormality in the peripheral metabolism of thyroxine in patients with active untreated Graves ' disease (1). In such patients, an abnormally large fraction of the extrathyroidal pool of thyroxine is degraded daily. Other authors have also observed an accelerated fractional turnover of thyroxine in patients with untreated Graves ' disease (2, 3) and have postulated that the rate of turnover of the hormone might be a function of its concentration in the blood (2). Alternatively, accelerated turnover of thyroxine might merely reflect the general speeding of metabolic processes which occurs during the hyperthyroid state. The present studies were designed to differentiate between these and other possibilities. Rates of turnover of thyroxine have been assessed in patients in whom the thyrotoxicity had been corrected by appropriate therapy, as well as in nonthyrotoxic subjects who were made hypermetabolic by the administration of thyroid hormone. A preliminary report of the data obtained has been published in abstract form (4). It has been shown that the induction of thyrotoxicosis medicamentosa does result in an augmentation of the fractional rate of turnover of thyroxine. However, it has also been demonstrated that accelerated fractional turnover of thyroxine frequently persists in patients with Graves ' disease, despit