Hepatic extraction and renal production of 3,3'-diiodothyronine and 3',5'-diiodothyronine in man.

Handling of iodothyronines by the liver and kidney in patients with chronic liver disease

“…The physiological relevance of these observations, however, is uncertain since a) significant effects required at least 250 µ /ml bovine TSH; b) type I deiodinase activity is im¬ paired in hypothyroid rats despite high plasma TSH, and c) liver and kidney cells do not possess TSH receptors. The percentage plasma 3,3'-T2 decrease across the liver was independent of the time after TRH administration and similar to that found by Faber et al (1980) under basal condi¬ tions. This all suggests that our findings are not influenced by the administration of TRH, al¬ though the rate-limiting steps in the metabolism of rT3 and 3,3'-T2 may be different (see below).…”

“…The mean ERPF in patient Nos. 7 and 8 was 396 the report of Faber et al (1980) in so far as these authors also found that rT3 and 3,3'-T2 concen¬ trations do not differ between arterial and peri¬ pheral venous blood. In addition, in healthy vol¬ unteers these authors estimated that hepatic ven¬ ous 3,3'-T2 levels are, on the average, 40% lower than the concentrations in arterial plasma.…”

“…This value is in excellent agreement with the 36% hepatic 3,3'-T2 gradient we measured in our group of patients. However, Faber et al (1980) also reported on a slight (7%) increase in renal vein 3,3'-T2 compared with arterial levels, which we observed only in 2 out of the 9 patients. It may be argued that this discrepancy is due to lowered type I deiodinase activity in patients with liver disease (Wartofsky & Burman 1982).…”

Alterations in 3,3'5'-triiodothyronine metabolism in response to propylthiouracil, dexamethasone, and thyroxine administration in man.

“…Less than 10% of labeled rT3 added to urine samples (29). This suggests that the human liver, sion like the rat liver, is also not a net producer of circulating rT3.…”

Circulating 3-T1AM and 3,5-T2 in Critically Ill Patients: A Cross-Sectional Observational Study

“…Athyreotic patients on L-T4 replacement therapy also had higher serum 3-T1AM concentrations than individuals with intact thyroid indicating its extrathyroidal formation from supplemented L-T4 (23). The TH metabolite 3,5-T2, which is theoretically formed through D1 deiodination of T3, has long been considered as a physiological inactive and minor metabolite of T4 and T3, but recent studies indicate that this metabolite might have a physiological impact on energy metabolism (24)(25)(26)(27)(28).…”