The acute influence of ingested thyroid hormones on hepatic deiodination pathways in the rainbow trout, Oncorhynchus mykiss.

Juvenile rainbow trout were fed once daily with trout pellets supplemented with L-thyroxine (T4) or 3,5,3'-triiodo-L-thyronine (T3) and the effects on plasma T4 and T3 levels and hepatic 5'-monodeiodinase (5'D) activity determined after 1, 2, or 3 days. In all cases T3 (12 ppm) elevated plasma T3 and caused a significant reduction in the functional level (Vmax) of 5'D with no change in enzyme affinity (Km). After 3 daily meals (3 ppm T3), 5'D activity fell to 52% of control levels. In most instances plasma T4 was increased. In contrast, ingestion of T4 for 3 days at levels up to 48 ppm did not modify hepatic 5'D. This may reflect either insensitivity of the 5'D system to T4 or poor T4 uptake from the gut, as plasma T4 levels were influenced to a small extent by T4 ingestion. HPLC analyses showed that dietary T3 supplements (0, 3, 6, or 12 ppm) for 3 days acted in a dose-dependent manner, not only to suppress T3 formation from T4 by outer-ring deiodination, but also to promote inner-ring deiodination of T4 to 3,3',5'-triiodo-L-thyronine (reverse T3) and outer-ring deiodination of T3. In conclusion, the present data indicate that in the face of a T3 challenge there is a rapidly responding hepatic autoregulation of T3 production, achieved by a complex coordinated regulation of several different iodothyronine deiodination pathways.