Serum Concentration, Metabolic Clearance, and Production Rates of 3,5,3′Triiodothyroacetic Acid in Normal and Athyreotic Man*

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Abstract
It has been demonstrated that 3,5,3′-triiodothyroacetic acid (Triac) is present in normal human serum. However, no quantitative assessment of its clearance rate (CR), production rate (PR), or the importance of extrathyroidal sources of Triac relative to direct thyroidal secretion is yet available. These parameters are here reported in five euthyroid subjects and eight athyreotic subjects (H) eumetabolic on T4 therapy (HT4; n = 5) or T3 (HT3; n = 3). The Triac concentration was determined by RIA in serum extracts. Each sample was corrected for recovery. The mean serum Triac concentration was 2.6 ± 0.2 ng/100 ml (mean ± SE) in 26 normal subjects. Triac was also detectable in serum from the HT4 and HT3 subjects (2.3 ± 0.2 and 3.8 ± 0.2 ng/100 ml, respectively). The latter value was significantly (P < 0.01) higher than the control mean. The Triac CR was determined from data acquired using an [125I]Triac constant infusion technique. Samples were analyzed by both anion exchange and Sephadex G-25F column chromatography. The serum concentrations of [125I]Triac were similar by both methods of analysis. In the control subjects, the Triac CR averaged 222 ± 37 liters/day, whereas the means were 198 ± 31 and 268 ± 4 liters/day in the HT4 and HT3 group, respectively. The Triac PR was calculated from the CR and serum concentration of Triac. The control mean PR at 5.2 ± 1.5 μg/day was similar to the HT4 mean of 4.4 ± 0.5 jug/day (all corrected to 70 kg BW). The mean Triac PR was significantly higher (P μ 0.025) in the HT3 group (10.1 ± 0.4 μg/day) compared to the control average. The mean molar ratio of the Triac PR to the daily T3 dose in the HT3 group was 0.14 ± 0.02. The similar Triac PR values in the controls and the HT4 group indicate that Triac is generated mainly from the extrathyroidal metabolism of T4 and that direct thyroidal secretion contributes little if at all to its daily production. The studies in the HT3 group indicate that alteration of the alanine side chain is an important pathway (14% of T3 degradation) in T3 degradation and that T3 is the major precursor of Triac in vivo.