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Rainbow trout held at 6.5°C were fed food supplemented with 12 ppm T3 (3,5,3′‐triiodo‐L‐thyronine). By 2 weeks, plasma T3 had increased from 3.7 ng/ml (controls) to 12 ng/ml and stayed at that level for 12 weeks with minor change in plasma L‐thyroxine (T4). The hepatic microsomal 5′‐deiodinase (5′‐D) activity (Vmax fell to 25% of control values by 2 weeks and by 12 weeks was undetectable. Trout were also fed the T3‐supplemented food for 6 weeks and then reverted to control food (0 ppm T3) for 6 weeks. After 2 weeks reversion, plasma T3 was 48% lower and 5′‐D Vmax 78% lower than for control fish fed 0 ppm T3 throughout; after 6 weeks reversion, plasma T3 had recovered, but 5′‐D had regained only 58% of control values. These data confirm that exogenous T3 suppresses endogenous T3 production and suggest extrathyroidal autoregulation of T3 production. Furthermore, even 6 weeks after T3 treatment had ceased, hepatic 5′‐D was subnormal, indicating development of T3 dependency.
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Eales et al. (1991) studied this question.
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