Endocrine Abstracts

Mice with combined deficiency in the thyroid hormone transporters Mct8 and Oatp1c1 (Mct8/Oatp1c1 dko mice) display a strongly diminished TH brain content and, consequently, a disturbed neuronal maturation and myelination as well as locomotor abnormalities while serum T3 levels are highly elevated. This phenotype can be explained by an impaired transport of T4 and T3 into the CNS in the absence of both transporters. Yet, the exact cell-specific function of Mct8 and Oatp1c1 in b...

Impaired TH transport across brain barriers results in severe TH deficiency in Mct8/Oatp1c1 DKO mice, leading to disturbed neuronal development, myelination as well as locomotor abnormalities. Although brain-barrier associated cells (i.e. endothelial cells, astrocytes, choroid plexus epithelial cells) have been shown to express both transporters, the cell-specific function of Mct8 and Oatp1c1 has still not been defined. Here, we generated and analysed mouse mutants that lack M...

Inactivation of the thyroid hormone transporters Mct8/Oatp1c1 in mice causes a profound TH deficiency in the CNS due to an impaired TH transport across brain barrier cells. As oligodendrocyte maturation and myelin formation requires proper thyroid hormone (TH) signaling, Mct8/Oatp1c1 double knock-out (DKO) mice exhibit a persistent state of hypomyelination similar to the situation in MCT8 deficient patients. Yet, to which extent proper myelination is dependent on the presence ...