Figure 1: Female mice are protected from diet-induced obesity and hypothalamic microglial activation.

(a,b) Body-weight gain (a) and cumulative food intake (b) in male and female mice exposed to chow or HFD for 18 weeks. (c,d) Total fat mass (c) and lean mass (d) in chow-fed and HFD groups. See also Supplementary Fig. 1. (e) Intraperitoneal glucose tolerance test (2 g kg⁻¹) in male and female mice after 18 weeks on chow or HFD. (f) Glucose AUC analysis of data from e. M, males; F, females. Data are presented as mean±s.e.m. of 12 males and 8 females per group in a–f. (g,h) mRNA levels of inflammatory markers in isolated hypothalamic microglia following 3-mo chow or HFD exposure (g: males; h: females). Data are presented as % change relative to chow-fed controls. Mean±s.e.m., n=8. *P<0.05 by Student’s t-test comparing within gender (i) CX3CL1 protein expression analysed by ELISA in homogenized hypothalamus dissected from male and female mice maintained on chow or HFD for 18 weeks. Data are presented as mean±s.e.m., n=8. (j,k) mRNA level of Cx3cr1 in isolated hypothalamic microglia following 3-mo chow or HFD exposure. Data are presented as per cent change relative to chow-fed controls. Mean±s.e.m., n=8. *P<0.05 by Student’s t-test comparing within gender. For all panels (except g,h,j,k), data are analysed by repeated measures or two-way ANOVA followed by Bonferroni post hoc comparisons. *P<0.05, **P<0.01 and ***P<0.001.