Effect of T3 Treatment and Food Ration on Hepatic Deiodination and Conjugation of Thyroid Hormones in Rainbow Trout, Oncorhynchus mykiss

Abstract

We studied the 7-day effects of 3,5,3′-triiodothyronine (T3) hyperthyroidism (induced by 12 ppm T3 in food) and food ration (0, 0.5, or 2% body weight/day) on in vitro hepatic glucuronidation, sulfation, and deiodination of thyroxine (T4), T3, and 3,3′,5′-triiodothyronine (rT3). T3 treatment doubled plasma T3 with no change in plasma T4, depressed hepatic low-Km (1 nM) outer-ring deiodination (ORD) of T4, induced low-Km (1 nM) inner-ring deiodination (IRD) of both T4 and T3 but did not alter high-Km (1 μM) rT3ORD, glucuronidation, or sulfation of T4, T3, or rT3. Plasma T4 levels were greater for 0 and 2% rations than for a 0.5% ration. Fasting decreased low-Km T4ORD activity and increased high-Km rT3ORD activity but did not alter T4IRD or T3IRD activities. T4, T3, and rT3 glucuronidation were greater for 0 and 0.5% rations than for a 2% ration. T3 glucuronidation was greater for a 0.5% ration than for a 0% ration. T3 and rT3 sulfation were greater for a 2% ration than for a 0 or a 0.5% ration; ration did not change T4 sulfation. We conclude that (i) modest experimental T3 hyperthyroidism induces T3 autoregulation by adjusting hepatic low-Km ORD and IRD activities but not high-Km rT3ORD or conjugation activities; (ii) in contrast, ration level changes both deiodination and conjugation pathways, suggesting that the response to ration does not solely reflect altered T3 production; (iii) deiodination and conjugation appear complementary in regulating thyroidal status in response to ration; and (iv) high-Km rT3ORD in trout differs from rat type I deiodination in that it does not respond to T3 hyperthyroidism and it increases, rather than decreases, its activity during fasting.