Abstract
Estradiol has well-known indirect effects on the thyroid. A direct effect of estradiol on thyroid follicular cells, increasing cell growth and reducing the expression of the sodium-iodide symporter gene, has been recently reported. The aim of the present investigation was to study the effect of estradiol on iodide uptake by thyroid follicular cells, using FRTL-5 cells as a model. Estradiol decreased basal iodide uptake by FRTL-5 cells from control levels of 2.490 +/- 0.370 to 2.085 +/- 0.364 pmol I-/microg DNA at 1 ng/ml (P<0.02), to 1.970 +/- 0.302 pmol I-/microg DNA at 10 ng/ml (P<0.003), and to 2.038 +/- 0.389 pmol I-/microg DNA at 100 ng/ml (P<0.02). In addition, 4 ng/ml estradiol decreased iodide uptake induced by 0.02 mIU/ml thyrotropin from 8.678 +/- 0.408 to 7.312 +/- 0.506 pmol I-/microg DNA (P<0.02). A decrease in iodide uptake by thyroid cells caused by estradiol has not been described previously and may have a role in goiter pathogenesis.
Highlights
Estradiol has a well-known indirect effect on thyroid function, increasing thyroxine-binding globulin, probably due to decreased clearance rather than increased production of thyroxine-binding globulin [1]
In the present study we examined the effect of estradiol on iodide uptake by FRTL5 cells
A direct effect of estradiol on thyroid follicular cells was expected because estrogen receptors are present in abundant amounts in these cells [7,8,9]
Summary
Estradiol has a well-known indirect effect on thyroid function, increasing thyroxine-binding globulin, probably due to decreased clearance rather than increased production of thyroxine-binding globulin [1]. A direct effect of estradiol increasing thyroid follicular cell growth and reducing the expression of the sodium-iodide symporter was recently described by one of us [3] but the net result of these actions on iodide uptake by thyroid cells is not known. The objective of the present investigation was to study the effect of estradiol on iodide uptake by thyroid follicular cells under basal conditions and after stimulation with thyrotropin (TSH), using FRTL-5 cells as a model [4]
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