Effect of Pharmacological Quantities of Infused 3,3′,5′- Triiodothyronine on Thyroxine Monodeiodination to 3,5,3′-Triiodothyronine*

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Abstract
The metabolic effects of rT3 and its role in regulating the metabolic activity of T4 by altering the peripheral monodeiodination of T4 to T3 was studied in normal and thyroidectomized (Tx) rats constantly infused through indwelling atrial catheters. The infusion of 100 μg rT3/100 g BW in normal rats decreased the conversion of T4 to T3 by liver homogenates by 50% (P < 0.001), decreased serum T3 by 21% (P < 0.001), increased serum T4 by 21% (P < 0.001) and had no effect on serum and pituitary GH concentrations. Tx rats were infused with saline, rT3 (100 μg/100 g BW), T4 (2–5 μg/100 g BW), T3 (1 μg/100 g BW), T4 plus rT3, and T3 plus rT3. The infusion of rT3 had no effect on serum and pituitary TSH and GH concentrations. T4 infusion in the Tx rat increased the low in vitro hepatic T3 generation observed in hypothyroidism, decreased serum TSH, increased serum and pituitary GH, and restored the metabolic effect of GH on the epididymal fat pad. The simultaneous infusion of rT3 and T4 partially blocked the metabolic effects of T4 in the Tx rat. Compared to T4 infusion alone, T4 plus rT3 decreased hepatic T3 generation (97%; P < 0.001), increased serum TSH (63%, P < 0.001), decreased serum T3 (41%; P < 0.005) and GH (57%; P < 0.01), decreased pituitary GH (40%, < 0.02), and prevented the in vivo effect of GH on the epididymal fat pad. A lower dose of rT3 (5 μg/100 g BW) did not alter the effects of T4. In contrast, the simultaneous infusion of rT3 with T3 did not effect the metabolic activity of T3. The present findings suggest that pharmacological doses of rT3 administered to the hypothyroid rat do not have thyroid hormone activity, as assessed by serum and pituitary TSH and GH concentrations and the peripheral effect of GH on epididymal fat. The constant infusion of large doses of rT3 impaired the hepatic conversion of T4 to T3, resulting in a decrease in the metabolic effectiveness of T4, but not T3, in the Tx rat. Since pharmacological concentrations or rT3 are required to inhibit T3 generation in vivo, it probable that rT3 has little if any physiological role in either the peripheral monodeiodination of T4 or the regulation of synthesis and secretion of TSH and GH by the pituitary. (Endocrinology106: 68, 1980)