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Endocrine Abstracts (2017) 49 S26.1 | DOI: 10.1530/endoabs.49.S26.1

ECE2017 Symposia Tissue specific defects in thyroid hormone action (3 abstracts)

Mouse models to study tissue specific hypothyroidism

Heike Heuer


Germany.


Thyroid hormone (TH) actions and metabolism are intracellular events that require the transport of TH across the plasma membrane in target cells. Consequently, impaired uptake of TH can lead to tissue- specific TH deprivation independent of the TH concentrations in the circulation. A prominent example for such a scenario represents the Allan-Herndon-Dudley syndrome (AHDS). This syndrome is caused by inactivating mutations in the X-linked Slc16a2 gene encoding the monocarboxylate transporter MCT8, a highly specific TH transporter widely expressed in CNS and peripheral tissues. Patients with inactive MCT8 display severe neurological symptoms and signs of brain hypothyroidism despite highly elevated serum T3 concentrations. Likewise, Mct8 ko mice exhibit abnormal TH serum values together with complex tissue-specific changes in the TH status ranging from hypothyroidism (brain, pituitary) to hyperthyroidism (liver, kidney, skeletal muscle). In order to define the tissue- specific function of Mct8 we recently started to generate mouse mutants that lack Mct8 in defined cell types only. In my presentation, I will report on our studies demonstrating pronounced cell-specific alterations in the TH status upon deletion of Mct8 at the blood-brain barrier (BBB), in hypothalamic tanycytes as well as in thyrocytes while absence of Mct8 in forebrain neurons or hepatocytes did not compromise proper tissue-specific TH action. Overall, our data clearly underscore the importance of Mct8 and other TH transporters in mediating TH transport thereby influencing tissue-specific TH homeostasis.

Volume 49

19th European Congress of Endocrinology

Lisbon, Portugal
20 May 2017 - 23 May 2017

European Society of Endocrinology 

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