Effect of T3 or T4 challenge on inner‐ and outer‐ring deiodination of T3 and T4 in the liver, kidney, and gill of rainbow trout, Oncorhynchus mykiss

Abstract

AbstractThe effects of feeding 3,5,3′‐triiodo‐L‐thyronine (T3)‐ and L‐thyroxine (T4)‐supplemented diets for 3 days on the plasma T3 and T4 concentrations and on the plasma outerring (5′D) and inner‐ring (5D) deiodination of T4 and T3 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. T3 treatment increased plasma T3 but did not alter plasma T4. T4 treatment did not alter plasma T3 or T4. In untreated trout, T45′D activity to form T3 occurred in all 3 tissues; T45D activity to form 3,3′,5′‐T3 (rT3) was not significant, T35D activity to form 3,3′‐T2 (diiodo‐L‐thyronine) was low, and T35′D activity to form 3,5‐T2 was barely detectable. A low‐Km T45′D (T4 concentration = 0.65 nM) was confirmed in liver and gill, and a high‐Km T45′D (T4 concentration = 12 nM) was confirmed in liver and kidney. For liver, T3 feeding depressed both low‐Km and high‐Km T45′D isozymes, but induced T45D and T35D; T4 feeding depressed only the high‐Km T45′D and increased T35′D slightly. For gill, T3 feeding depressed the low‐Km T45′D and induced T45D; T4 feeding increased T35′D. For kidney, T3 feeding depressed the high‐Km T45′d and induced T35′D; T4 feeding depressed the high‐Km T45′D and increased T35′D. We conclude that in response to either a T3 or a T4 challenge, trout tissues employ several T3 homeostatic mechanisms. Responses to a T3 challenge included (1) depression of both low‐Km and high‐Km T45′D activities to decrease production of T3, (2) elevation of T45D activity to direct T4 substrate to rT3, and (3) elevation of T35D activity to degrade T3 to 3,3′‐T2. In contrast, responses to a 4‐fold greater dietary T4 challenge were restricted primarily to depression of high‐Km T45′D activity in the liver and kidney. © 1993 Wiley‐Liss, Inc.