Effect of T(3) treatment and food ration on hepatic deiodination and conjugation of thyroid hormones in rainbow trout, Oncorhynchus mykiss.

We studied the 7-day effects of 3,5,3'-triiodothyronine (T(3)) hyperthyroidism (induced by 12 ppm T(3) in food) and food ration (0, 0.5, or 2% body weight/day) on in vitro hepatic glucuronidation, sulfation, and deiodination of thyroxine (T(4)), T(3), and 3,3', 5'-triiodothyronine (rT(3)). T(3) treatment doubled plasma T(3) with no change in plasma T(4), depressed hepatic low-K(m) (1 nM) outer-ring deiodination (ORD) of T(4), induced low-K(m) (1 nM) inner-ring deiodination (IRD) of both T(4) and T(3) but did not alter high-K(m) (1 microM) rT(3)ORD, glucuronidation, or sulfation of T(4), T(3), or rT(3). Plasma T(4) levels were greater for 0 and 2% rations than for a 0.5% ration. Fasting decreased low-K(m) T(4)ORD activity and increased high-K(m) rT(3)ORD activity but did not alter T(4)IRD or T(3)IRD activities. T(4), T(3), and rT(3) glucuronidation were greater for 0 and 0.5% rations than for a 2% ration. T(3) glucuronidation was greater for a 0.5% ration than for a 0% ration. T(3) and rT(3) sulfation were greater for a 2% ration than for a 0 or a 0.5% ration; ration did not change T(4) sulfation. We conclude that (i) modest experimental T(3) hyperthyroidism induces T(3) autoregulation by adjusting hepatic low-K(m) ORD and IRD activities but not high-K(m) rT(3)ORD 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 T(3) production; (iii) deiodination and conjugation appear complementary in regulating thyroidal status in response to ration; and (iv) high-K(m) rT(3)ORD in trout differs from rat type I deiodination in that it does not respond to T(3) hyperthyroidism and it increases, rather than decreases, its activity during fasting.