Abstract
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.
Highlights
To sympathetic stimulation[11,12]
In mice centrally administered T3 leads to the recruitment of BAT in inguinal WAT which is accompanied by increased energy expenditure and body temperature
LXRαβ−/− mice display increased Thyroid hormones (TH) serum level combined with changes in expression of genes associated with TH synthesis and TH transport as well as prominent UCP1 staining in the subcutaneous adipose depot[26]
Summary
To sympathetic stimulation[11,12]. This suggests that the subsequent heat liberation is a result of synergism between norepinephrine (NE) and T3 signaling[13]. With regards to WAT, a distinct population of UCP1-positive adipocytes arises within subcutaneous and visceral depots of mice in response to cold exposure[15,16] and β3 adrenergic receptor agonist treatment[15,17,18]. To date it remains a matter of controversy as to whether these cells, entitled “brite” or “beige” adipocytes, are produced from the conversion of existing white adipocytes and/or the differentiation of WAT resident progenitor cells, leading to a process called “browning”[19,20,21]. The present study aimed to determine TH induced effects on (I) BAT activity and (II) WAT browning in a mouse model of thyroidal dysfunction with a view to incorporate the results into the context of TH-regulated effects on whole-body energy homeostasis
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