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Figure 3

From: Brown adipose tissue dysfunction promotes heart failure via a trimethylamine N-oxide-dependent mechanism

Figure 3

Choline and trimethylamine N-oxide are increased in heart failure. (A) Changes of cationic metabolites in BAT from mice at 2 weeks after TAC or sham surgery (Sham) assessed by CE-TOF/MS. Results of some metabolites are also shown in Fig. 3B as a box plot panel. (B) Tissue weight-adjusted levels of choline (n = 5, 5) or phosphorylcholine (n = 5, 5) in BAT from mice at 2 weeks after Sham or TAC. (C) Plasma choline level in mice with implantation of WAT or BAT (n = 5, 5). (D, E) Plasma (D) or myocardial (E) trimethylamine N-oxide (TMAO) level in mice at 2 weeks after sham or TAC (n = 11, 11). (F, G) Plasma (F) or heart (G) TMAO level in sham and BATectomy model mice 2 weeks after TAC (n = 3, 5). (H) TMAO levels in myocardium (left) and plasma (right) of WT mice treated with PBS (Con) or TMAO mice for 2 weeks (n = 5, 5). (I) Cardiac function of mice at 2 weeks after Sham or TAC with/without TMAO treatment (n = 7, 7, 19, 16). (J) Masson’s trichrome staining of hearts from mice in (I). The right panel shows quantification of the fibrotic area (n = 7, 7, 21, 17). Scale bar = 50 μm. (K) Plasma choline level (left panel) and TMAO level (right panel) in control subjects (Con) or patients with CHF (n = 23, 30). Data were analysed by the 2-tailed Student’s t-test (A–H and K) or 2-way ANOVA followed by Dunnett’s comparison test (I and J). *P < 0.05, **P < 0.01. Values are shown as the mean ± s.e.m.

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