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Endocrine Abstracts (2014) 35 OC7.5 | DOI: 10.1530/endoabs.35.OC7.5

1Universität zu Lübeck, Medizinische Klinik I, Lübeck, Germany; 2Leibniz-Institut für Nutztierbiologie, Dummerstorf, Germany.


Introduction: Thyroid hormones (TH) are essential regulators of metabolism and increase energy expenditure (EE). Mitochondria-rich brown adipose tissue (BAT) is specialised in thermogenesis and significantly contributes to EE. BAT contains essential components of TH action but TH transporters like MCT8 have not been characterised so far. As direct effects on O2 consumption and mitochondrial action have not been investigated before we tested MCT8 expression and direct effects of T3 in a BAT cell line.

Methods: We treated our previously described immortalised murine BAT cell line with triiodothyronine (T3) for 24h, determined MCT8 expression, and assessed aspects of mitochondrial function using immunohistochemistry, western blotting, ADP/ATP measurements, electron microscopy (EM) and oxygen consumption.

Results: Brown adipocytes express MCT8 transporters immunohistochemically. Administration of T3 did not cause any ultrastructural changes of mitochondria, as analysed by EM. Using western blotting with specific antibodies targeting TOMM20 and ATP synthase subunit beta, mitochondrial mass did not change. Mitochondrial autophagy as monitored by BNIP3 protein levels decreased slightly whereas PGC1alpha, a master regulator of mitochondrial biology, increased significantly. Oxygen consumption increased significantly and time-dependently upon T3 treatment and inner mitochondrial membrane potential decreased in parallel. No relevant alterations of ADP and ATP concentrations were detected.

Conclusions: This is a first functional demonstration of a direct T3 action on mitochondrial physiology in BAT cell lines, which express all components for T3 action including the TH transporter MCT8. Our data correspond well with metabolic adaptions seen after systemic TH treatment of rodents and humans and indicate an important effect of T3 independent of the central nervous system.

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