Iodothyronine deiodinases and the control of plasma and tissue thyroid hormone levels in hyperthyroid tilapia (Oreochromis niloticus)
Journal of Endocrinology
Thyroid status is one of the most potent regulators of peripheral thyroid hormone metabolism in vertebrates. Despite this, the few papers that have been published concerning the role of thyroid hormones in the regulation of thyroid function in fish often offer conflicting data. We therefore set out to investigate the effects of tetraiodothyronine (thyroxine) (T 4 ) or tri-iodothyronine (T 3 ) supplementation (48 p.p.m.) via the food on plasma and tissue thyroid hormone levels as well as
... as well as iodothyronine deiodinase (D) activities in the Nile tilapia (Oreochromis niloticus). T 4 supplementation did not induce a hyperthyroid state and subsequently had no effects on the thyroid hormone parameters measured, with the liver as the sole notable exception. In T 4 -fed tilapias, the hepatic T 4 levels increased substantially, and this was accompanied by an increase in in vitro type I deiodinase (D1) activity. Although the lack of effect of T 4 supplementation could be partially explained by an inefficient uptake of T 4 from the gut, our current data suggest that also the increased conversion of T 4 into reverse (r)T 3 by the D1 present in the liver plays an important role in this respect. In addition, T 3 supplementation increased plasma T 3 and decreased plasma T 4 concentrations. T 3 levels were also increased in the liver, brain, kidney, gill and white muscle, but without affecting local T 4 concentrations. However, this increase in T 3 availability remained without effect on D1 activity in liver and kidney. This observation, together with the 6-n-propylthiouracyl (PTU) insensitivity of the D1 enzyme in fish, sets the D1 in teleost fish clearly apart from its mammalian and avian counterparts. The changes in hepatic deiodinases confirm the role of the liver as an important T 3 -regulating tissue. However, the very short plasma half-life of exogenously administered T 3 implies the existence of an efficient T 3 clearing/degradation mechanism other than deiodination.