Extended Data Fig. 9: TEL promotes iWAT browning and energy expenditure.
From: BCAA–BCKA axis regulates WAT browning through acetylation of PRDM16
(a) Energy expenditure was analyzed by ANCOVA, with body weight included as a covariate. n=5 mice. (b-c) TEL increases body temperature under cold exposure but not room temperature. The representative rectal temperatures were shown. n=5 (Control) and n=6 (TEL). (d) Temperature at interscapular area of TEL treated mice is significantly higher than that of control mice showed by thermal infrared imaging. n=4 mice. (e) TEL upregulates thermogenesis related gene expression. n=6. (f) TEL increases Cidea expression in iWAT. Cidea protein levels as indicated were quantified and normalized against Tubulin. n=3. (g) TEL increases Ucp1 expression in BAT. Representative images of Ucp1 immunohistochemistry (IHC) in BAT from mice fed with HFD. Representative result from 4 mice. (h) TEL decreases body weight of obesity mice. n=5 mice. (i) GTT and ITT data from HFD and telmisartan group. n=5 mice. (j) Fat tissue weights of HFD and TEL group mice. n=6 mice. (k) TEL upregulates Ucp1 expression. TEL was given post obesity. Ucp1 protein levels as indicated were quantified and normalized against Tubulin. n=5. Bars and error bars represent mean values and SDs, with biologically individual data points shown. P values are derived from unpaired, two-tailed t-test (b, d, e, j), or repeated-measures 2-way ANOVA followed by Sidak’s multiple-comparison test (c, h, i). Energy expenditure in Fig.a was analyzed by ANCOVA, with body weight included as a covariate.
