SLCO1C1 and tyrosine hydroxylase deficiency: Overall, attempting to increase transplacental maternal-fetal TH transport and to protect the feto-placental unit from lower circulating TH levels in the case of iodine and TH deficiency, a compensatory mechanism in placenta before the onset of fetal thyroid function is largely facilitated by placental Oatp1c1 with a minor role played by D2 and D3.