Fig. 4

Agrp neurons promote lipogenesis. a Control (black) and Agrp^Trpv1 (blue) mice were injected with capsaicin. b NEFA levels (interaction: F_2, 54 = 3.91, P = 0.02; time: F_2, 54 = 9.64, P = 0.0003; genotype: F_1, 27 = 1.74, P = 0.19; MCT: P_80 min = 0.03). c Blood glucose levels (interaction: F_2, 54 = 1.47, P = 0.23; time: F_2, 54 = 14.6, P < 0.0001; genotype: F_1, 27 = 0.67, P = 0.41; MCT: ns). In b and c: control (n = 15) and Agrp^Trpv1 mice (n = 14). Statistics: two-way analysis of variance (ANOVA) with time as a repeated measure followed by Holm–Sidak’s multiple comparisons test (MCT). d Gene expression in the WAT. Data are normalized to control levels (dashed line). Statistics: Student’s t-test. *P < 0.05. e Western blotting analysis of phosphorylated HSL in inguinal WAT and retroperitoneal WAT (n = 4 mice per group). Blots were cropped for clarity. Statistics: Student’s t-test. *P < 0.05. f Control and Agrp^Trpv1 mice randomly received vehicle or the FAS inhibitor (C75, 10 mg kg⁻¹, intraperitoneal (i.p.)) immediately before capsaicin injection. g–i Respiratory exchange ratio (RER) (interaction: F_1, 26 = 4.36, P = 0.04; drug: F_1, 26 = 22.28, P < 0.0001; genotype: F_1, 26 = 11.73, P = 0.002). j–l Fat utilization (interaction: F_1, 26 = 9.97, P = 0.04; drug: F_1, 26 = 6.00, P = 0.02; genotype: F_1, 26 = 6.56, P = 0.01). m–o Carbohydrate utilization: (interaction: F_1, 26 = 12.18, P = 0.001; drug: F_1, 26 = 0.76, P = 0.38; genotype: F_1, 26 = 4.90, P = 0.03). In g–o, statistics: two-way ANOVA on the mean response after drug and capsaicin injection; genotype and drug as factors for the ANOVA. Holm–Sidak’s multiple comparisons test (MCT) was used and indicated as *P < 0.05, **P < 0.01, ***P < 0.001 and ****P < 0.0001. Control mice + vehicle (n = 8); control mice + C75 (n = 8); Agrp^Trpv1 mice + vehicle (n = 7); Agrp^Trpv1 mice + C75 (n = 7). Dashed line indicates time of injections. Colored symbols indicate mean ± SEM. Gray symbols indicate individual values