Abstract
The effects of feeding 3,5,3′‐triiodo‐L‐thyronine (T~3~)‐ and L‐thyroxine (T~4~)‐supplemented diets for 3 days on the plasma T~3~ and T~4~ concentrations and on the plasma outerring (5′D) and inner‐ring (5D) deiodination of T~4~ and T~3~ were studied in vitro for the liver, gill, and kidney of rainbow trout (Oncorhynchus mykiss) at 12°C. Trout were sampled 24 hr after their last meal. T~3~ treatment increased plasma T~3~ but did not alter plasma T~4~. T~4~ treatment did not alter plasma T~3~ or T~4~. In untreated trout, T~4~5′D activity to form T~3~ occurred in all 3 tissues; T~4~5D activity to form 3,3′,5′‐T~3~ (rT~3~) was not significant, T~3~5D activity to form 3,3′‐T~2~ (diiodo‐L‐thyronine) was low, and T~3~5′D activity to form 3,5‐T~2~ was barely detectable. A low‐K~m~ T~4~5′D (T~4~ concentration = 0.65 nM) was confirmed in liver and gill, and a high‐K~m~ T~4~5′D (T~4~ concentration = 12 nM) was confirmed in liver and kidney. For liver, T~3~ feeding depressed both low‐K~m~ and high‐K~m~ T~4~5′D isozymes, but induced T~4~5D and T~3~5D; T~4~ feeding depressed only the high‐K~m~ T~4~5′D and increased T~3~5′D slightly. For gill, T~3~ feeding depressed the low‐K~m~ T~4~5′D and induced T~4~5D; T~4~ feeding increased T~3~5′D. For kidney, T~3~ feeding depressed the high‐K~m~ T~4~5′d and induced T~3~5′D; T~4~ feeding depressed the high‐K~m~ T~4~5′D and increased T~3~5′D. We conclude that in response to either a T~3~ or a T~4~ challenge, trout tissues employ several T~3~ homeostatic mechanisms. Responses to a T~3~ challenge included (1) depression of both low‐K~m~ and high‐K~m~ T~4~5′D activities to decrease production of T~3~, (2) elevation of T~4~5D activity to direct T~4~ substrate to rT~3~, and (3) elevation of T~3~5D activity to degrade T~3~ to 3,3′‐T~2~. In contrast, responses to a 4‐fold greater dietary T~4~ challenge were restricted primarily to depression of high‐K~m~ T~4~5′D activity in the liver and kidney. © 1993 Wiley‐Liss, Inc.