Fig. 3: PLT3 potently stimulates energy expenditure and thermogenesis in WAT by avoiding feedback inhibition of adrenergic input to WAT.

Male C57BL/6 N mice on HFD for 8 weeks were IP administered with different forms of T3 or saline for 32 days and then subjected to analysis with the Comprehensive Lab Animal Monitoring System (CLAMS). a Whole-body oxygen consumption rate (VO₂) of mice during 72-h light/dark cycles. b Regression plots of VO₂ against body weight. c ANCOVA-predicted whole-body VO₂ at the mean body weight (50.14 g) of saline-treated mice. d, e Respiratory exchange ratio (RER) of mice. Blank and black boxes above the X axis represent light and dark phases respectively in (a) and (d). f Oxygen consumption rates (OCRs) in various tissues were measured by a Seahorse bioanalyzer. g Representative infrared thermography and h quantification of the skin temperature surrounding iWAT (black circles). i Representative infrared thermography and j quantification of the skin temperature surrounding iBAT (black circles). k The abundance of protein expression of throsine hydroxylase (THA) determined by western blot and l densitometry quantification of THA protein in iWAT and iBAT. m Norepinephrine content, n cyclic adenosine monophosphate (cAMP) content, and o free fatty acid (FFA) content in iWAT and iBAT. a–e, g–j n = 7 (Saline and FT3) or 8 (LT3 and PLT3) biologically independent replicates from one experiment. f n = 5 biologically independent replicates from one experiment. k, l n = 3 biologically independent replicates from one experiment. m–o n = 15 (Saline and FT3) or 16 (LT3 and PLT3) biologically independent replicates from three independent experiments. All data are expressed as mean ± SEM. One-way ANOVA followed by LSD test was applied for comparisons among multiple groups. All the p values were two-sided. Source data are available as a Source Data file.