Figure 4. Afferent vagal fibers contribute to SNS–driven dysfunctions in Vav3^–/– mice.

(A–C) Mean arterial pressure (A), heart frequency (B), and breathing ratio (C) of mice of the indicated genotypes (inset) and experimental conditions (bottom).

(D) Glucose tolerance test of the animals of the indicated genotypes and experimental groups.

(E) Area under the curve values for the experiments shown in (D).

(F) Quantification of triglycerides in liver extracts from mice of the indicated genotypes and experimental groups.

(G,H) Abundance of the indicated transcripts in liver (G) and WAT (H) extracts from mice of the indicated genotypes and experimental groups. Bic, bicuculline.

(I) Representative histological images of interscapular BAT sections from mice of indicated genotypes and experimental groups. Scale bar = 100 μm.

(J) Quantification of the number of brown adipocytes per field in interscapular BAT from experiments shown in (I).

(K) Abundance of the indicated transcripts in BAT extracts from mice of the indicated genotypes and experimental groups. WT–S, sham operated WT mice; WT–AV, WT mice with afferent vagotomy; V3–S, sham operated Vav3^–/– mice; Vav3–AV, Vav3^–/– mice with afferent vagotomy.

(L) Summary of the results obtained in this work. Stimulatory and inhibitory connections are depicted as arrows and blunted lines, respectively.

Data shown in panels A–H, J and K represent mean ± SEM. *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001 relative to either sham operated WT (black asterisks) or the sham operated animals of the same genotype group (red and green asterisks). Student’s t, ANOVA, and Mann–Whitney U tests were used for data obtained in panels (A–E,J), (G), and (F,H,K), respectively. n = 11 (sham operated WT mice), 11 (sham operated Vav3^–/– mice), 5 (sham operated Vav2^–/– mice), 12 (vagotomized WT mice), 15 (vagotomized Vav3^–/– mice), 6 (vagotomized Vav2^–/– mice).