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The hormone 1,25-dihydroxyvitamin D₃ (1,25-(OH)₂D₃) has been shown to selectively enhance agonist-induced TSH release in the rat thyrotroph in vitro. The interaction of 1,25-(OH)₂D₃ with tri-iodothyronine (T₃) and cortisol was studied in primary cultures of dispersed anterior pituitary cells. TRH (1 nmol/l)-induced TSH release over 1 h was enhanced by 70% (P<0·01) following exposure to 10 nmol 1,25-(OH)₂D₃/l for 24 h. Pretreatment with T₃ (1 pmol/l–1 µmol/l) for 24 h caused a dose-dependent inhibition of TRH-induced TSH release. Net TRH-induced TSH release was inhibited by 85% at T₃ concentrations of 3 nmol/l or greater. Co-incubation with 1,25-(OH)₂D₃ resulted in enhanced TRH-induced TSH release at all T₃ concentrations tested (P<0·001). The increment of TRH-induced TSH release resulting from 1,25-(OH)₂D₃ pretreatment was equivalent in the presence or absence of maximal inhibitory T₃ concentrations. At 1 nmol T₃/1, there was a two- to threefold relative increase in 1,25-(OH)₂D₃-enhanced TRH-induced TSH release. Incubation with cortisol (100 pmol/l–100 nmol/l) had no effect on basal or TRH-induced TSH release, nor did it alter 1,25-(OH)₂D₃-enhanced TRH-induced TSH release when added 24 h before, or at the time of addition of 1,25-(OH)₂D₃. Actinomycin D and -amanitin abolished 1,25-(OH)₂D₃-enhanced TSH secretion.

These data demonstrate that the action of 1,25-(OH)₂D₃ in the thyrotroph required new RNA transcription, and was not affected by cortisol. In the presence of T₃, the response of the thyrotroph to TRH induced by 1,25-(OH)₂D₃ was increased. We have shown that 1,25-(OH)₂D₃ has significant effects on the action of TRH and T₃ in vitro. These findings support the proposal that 1,25-(OH)₂D₃ may modulate TSH secretion in vivo.

Journal of Endocrinology (1989) 121, 451–458