1,25-Dihydroxycholecalciferol attenuates thyrotropin stimulated iodide accumulation in rat thyroid follicular FRTL-5 cells by reducing iodide porter number.
We have recently shown that rat thyroid follicular FRTL-5 cells have functional receptors for 1,25-dihydroxycholecalciferol (1,25- (OH)2D3) and that 1,25-(OH)2D3 attenuates the thyrotropin (TSH) induced iodide uptake. Here we show that the dibutyrylcyclic AMP induced iodide uptake was significantly reduced by 1,25-(OH)2D3, indicating that 1,25-(OH)2D3 affects the cAMP signal pathway beyond cAMP generation. The Vmax of the iodide porter was significantly reduced in 1,25-(OH)2D3 treated cells as compared to cells treated with TSH alone, indicating that 1,25-(OH)2D3 reduces the effective number of iodide porters in FRTL-5 cells.
Lamberg-Allardt
C
C
Endocrine Research Laboratory, University of Helsinki, Finland.
Valtonen
E
E
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D003994:Bucladesine / Q000494:pharmacology; D002117:Calcitriol / Q000494:pharmacology*; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D007454:Iodides / Q000378:metabolism*; D007700:Kinetics; D051381:Rats; D013961:Thyroid Gland / Q000187:drug effects / Q000378:metabolism*; D013972:Thyrotropin / Q000037:antagonists & inhibitors / Q000494:pharmacology*
D007454:Iodides; D003994:Bucladesine; D013972:Thyrotropin; D002117:Calcitriol