Key result
Long-term T3 increases brown fat thermogenic capacity in mice via progenitor cell proliferation.
Why the study?
The thyroid hormone-controlled recruitment process of brown adipose tissue is not fully understood.
Caution against clinical T3 use for thermogenesis; leaves open human translation of TRα-driven BAT progenitor proliferation.
The thyroid hormone (TH)-controlled recruitment process of brown adipose tissue (BAT) is not fully understood. Here, we show that long-term treatment of T3, the active form of TH, increases the recruitment of thermogenic capacity in interscapular BAT of male mice through hyperplasia by promoting the TH receptor α-mediated adipocyte progenitor cell proliferation. Our single-cell analysis reveals the heterogeneous nature and hierarchical trajectory within adipocyte progenitor cells of interscapular BAT. Further analyses suggest that T3 facilitates cell state transition from a more stem-like state towards a more committed adipogenic state and promotes cell cycle progression towards a mitotic state in adipocyte progenitor cells, through mechanisms involving the action of Myc on glycolysis. Our findings elucidate the mechanisms underlying the TH action in adipocyte progenitors residing in BAT and provide a framework for better understanding of the TH effects on hyperplastic growth and adaptive thermogenesis in BAT depot at a single-cell level.
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Liu et al. (2022) studied Brown adipose tissue recruitment. Triiodothyronine (T3) vs. PBS or no T3 was evaluated on Thermogenic capacity and adipocyte progenitor cell proliferation in interscapular brown adipose tissue. Long-term treatment with Triiodothyronine (T3) increases the recruitment of thermogenic capacity in interscapular brown adipose tissue of male mice through hyperplasia by promoting thyroid hormone receptor α-mediated adipocyte progenitor cell proliferation.
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