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Female rainbow trout were rendered either hypothyroid by ipodate injection or hyperthyroid by immersion in a 3,5,3′‐triiodo‐L‐thyronine (T 3 ) solution or by feeding T 3 ‐supplemented pellets, and ovarian function was evaluated from the gonadosomatic index (gonad weight .10 2 . body weight −1 = GSI), plasma 17β‐estradiol (E 2 ) level, or the ability in vitro of ovarian pieces to release E 2 in the presence of salmon gonadotropin (sGtH). Hypothyroidism for 7 or 22 days depressed GSI or in vitro ovarian E 2 release. Modest hyperthyroidism for 7 or 22 days, which raised plasma T 3 from 1.6–3.3 ng/ml (controls) to 4.1–7.7 ng/ml, significantly increased GSI and in vitro ovarian E 2 release. However, at higher T 3 levels (21–33 ng/ml) there was no increase in GSI and either no increase or a significant decrease in ovarian E 2 release. None of these treatments altered the plasma E 2 levels although T 3 treatment significantly enhanced the effect of injected sGtH in elevating E 2 level. It is concluded that T 3 at physiologic levels enhances ovarian growth and GtH stimulation of E 2 production, but when plasma T 3 levels exceed those required to saturate putative T 3 receptor sites, T 3 tends to inhibit ovarian function.
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Cyr et al. (1988) studied this question.
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