Fig. 5

Adipose tissue endocannabinoid metabolism mediates the appetite-inducing effect of OGT. a Heatmap of N-acylethanolamine (NAE) profiles in adipose tissue (pgWAT) and serum from mice (n = 8 per group) fed HFD or mHFD for 14–15 weeks. Data has been processed to follow Gaussian distribution. Each box represents the log₂ ratio of FKO/WT. b, c Levels of AEA in adipose tissue (b) and serum (c) from mice described above. d Energy intake of mice (n = 15 or 11) fed HFD for 10–13 weeks and dosed with FAAH inhibitor URB597 (0.5 mg/kg). n.s. not significant, *P < 0.05, multiple t-tests adjusted by the Holm–Sidak method. e Energy intake of mice (n = 11 or 10) fed HFD for 12–14 weeks and dosed with CB1 agonist ACEA (1 mg/kg). Mice were dosed at 8:30–9:00 a.m., and measured at indicated time points. n.s. not significant, *P < 0.05, **P < 0.01, repeat-measure post hoc Sidak’s tests. f Energy intake of mice (n = 7 per group) fed HFD for 13 weeks dosed with peripheral CB1 receptor blocker AM 6545 as indicated. Data were presented as mean ± s.e.m. n.s. not significant, *P < 0.05, **P < 0.01, ****P < 0.0001, post hoc Sidak’s tests, or ^#P < 0.05, two-tailed Student’s t-test. g Food intake (% pre-injection baseline) of mice (n = 11 or 10) fed HFD for 10–11 weeks and dosed with CB1 antagonist AM 6545 (3.5 mg/kg). **P < 0.01, repeat-measure post hoc Sidak’s tests. A dashed line in (b, c) indicates that data from HFD study and mHFD study are presented in a side-by-side manner, and inference may not be made between different diets