Extended Data Fig. 6: BCKA rescue phenotype induced by Bcat2 KO.
From: BCAA–BCKA axis regulates WAT browning through acetylation of PRDM16
(a) BCKA (KMV and KIC, not including KIV) was supplemented in drinking water at 0.5,1 and 2 mg/ml. Body weight data are showed under HFD. n=5 mice. (b) BCKA supplement doesn’t affect body weight. n=5 mice. (c) BCKA supplement doesn’t affect water intake. Representative mean value from 5 mice in a cage. (d) BCKA supplement doesn’t affect food intake. Representative mean value from 5 mice in a cage. (e) BCKA (KMV and KIC, not including KIV) supplement increase KMV and KIC concentrations in serum. n=3 mice. (f) BCKA supplement rescues body weight. n=5 mice. (g) BCKA restore Bcat2 KO-decreased glucose intolerance and insulin tolerance. n=5 mice. (h) BCKA supplement rescues fatty liver. Representative result from 4 mice. (i) BCKA supplement increase KMV and KIC concentrations in iWAT. n=3 mice. (j) BCKA restore Bcat2 KO-increased Cidea expression in iWAT. Cidea protein levels as indicated were quantified and normalized against Tubulin. n=3 mice. (k) The acetylation level of Prdm16 from BAT. The acetylation level of Prdm16 was normalized against immunoprecipitated Prdm16 protein as indicated. n=3 mice. (l) Ac-CoA level decreases in BAT from Bcat2 Adipose KO mice. n=3 biological independent experiments. (m-n) Ucp1, Prdm16 and Pgc1α expression levels of iWAT and BAT. The protein levels as indicated were quantified and normalized against Tubulin. n=3 mice (m) and n=6 mice (n). 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 (except a and g), or repeated-measures 2-way ANOVA followed by Sidak’s multiple-comparison test (Fig. a and g).
