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Sci Rep. 2016 Dec 12;6:38124. doi: 10.1038/srep38124.

Thyroid hormone status defines brown adipose tissue activity and browning of white adipose tissues in mice.

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Department of Endocrinology and Nephrology, University Hospital, Leipzig, Germany.
Helmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Research Site Leipzig, Department of Neuroradiopharmaceuticals, Leipzig, Germany.
University of Leipzig, IFB Adiposity Diseases, Leipzig, Germany.
German Center for Diabetes Research (DZD), Leipzig, Germany.
Department of Nuclear Medicine, University Hospital, Leipzig, Germany.
Institute of Experimental Endocrinology, Charité University Hospital, Berlin, Germany.


The present study aimed to determine the effect of thyroid hormone dysfunction on brown adipose tissue activity and white adipose tissue browning in mice. Twenty randomized female C57BL/6NTac mice per treatment group housed at room temperature were rendered hypothyroid or hyperthyroid. In-vivo small animal 18F-FDG PET/MRI was performed to determine the effects of hypo- and hyperthyroidism on BAT mass and BAT activity. Ex-vivo14C-acetate loading assay and assessment of thermogenic gene and protein expression permitted analysis of oxidative and thermogenic capacities of WAT and BAT of eu-, hyper and hypothyroid mice. 18F-FDG PET/MRI revealed a lack of brown adipose tissue activity in hypothyroid mice, whereas hyperthyroid mice displayed increased BAT mass alongside enhanced 18F-FDG uptake. In white adipose tissue of both, hyper- and hypothyroid mice, we found a significant induction of thermogenic genes together with multilocular adipocytes expressing UCP1. Taken together, these results suggest that both the hyperthyroid and hypothyroid state stimulate WAT thermogenesis most likely as a consequence of enhanced adrenergic signaling or compensation for impaired BAT function, respectively.

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