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Evaluation of TRIAC activity in Mct8 KO mice

AuthorsBárez-López, Soledad; Obregón, María Jesús; Martínez de Mena, Raquel ; Bernal, Juan ; Guadaño-Ferraz, Ana ; Morte, Beatriz
Issue Date2014
CitationETA 2014
AbstractThe monocarboxylate transporter 8 (MCT8) is a thyroid hormone (TH)-specific cell membrane transporter that is essential for T3 transport to the brain. MCT8 mutations lead to severe neurological impairments and abnormal serum TH levels. To date, therapeutic options for patients with MCT8 mutations are limited. The acetic acid derivative of T3 TRIAC has potential therapeutic value. Here we have analysed the in vivo effects of TRIAC on wild type (WT) and Mct8 knockout (KO) mice after administration of 30 ng/g bw/day in the drinking water from P21 to P30. TRIAC, T4 and T3 were measured by specific RIAs. Serum TRIAC reached the same concentration in WT and Mct8KO after treatment. TRIAC treatment greatly decreased serum T4 in the WT and the Mct8KO, and decreased T3 to normal levels in the Mct8KO. Serum T3 did not change in the WT after treatment. Liver D1 activity and mRNA were increased after TRIAC treatment in both genotypes. To assess the effect of TRIAC on the brain we measured D2 activity and the expression of the TH-regulated genes Hr, Cbr2, Itih3, and Flywch2 in the cerebral cortex. D2 activity was elevated in the Mct8KO, and did not change after treatment, in correspondence with the low circulating T4. There were no effects of TRIAC on Hr, Cbr2, and Itih3 expression, but Flywch2 was reduced in the Mct8KO. The results indicate that TRIAC treatment induced a state of hypothyroidism partially compensated by its thyromimetic actions on peripheral tissues.
DescriptionResumen del póster presentado al 38th Annual Meeting of the European Thyroid Association celebrado en Santiago de Compostela (España) del 6 al 10 de septiembre de 2014.-- et al.
Appears in Collections:(IIBM) Comunicaciones congresos
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