Figure 1: RIIβ KO mice show enhanced response to leptin.

(a) Serum leptin levels of 12-week-old age-matched male wild-type (WT) (n=7) and RIIβ KO mice (n=9). (b) Hypothalamic Npy (fed WT n=6, KO n=8; fasted WT n=11, KO n=11), Agrp (fed WT n=5, KO n=5; fasted WT n=11, KO n=11) and Pomc mRNA (fed WT n=6, KO n=8; fasted WT n=11, KO n=11) from fed and fasted male WT and RIIβ KO mice. Messenger RNA values were determined by quantitative reverse transcription–PCR and standardized to LepRb mRNA. Fed WT mice were set at one in all cases. For each group of mice, n=5–11. (c) 24-h food intake change in male WT (n=5) and RIIβ KO mice (n=5) in response to 500 or 100 ng leptin i.c.v. administration into the third ventricle. (d) Changes in daily food intake and (e) body weight of male WT (n=7) and RIIβ KO (n=11) mice over 13 days following vehicle or leptin i.c.v. injections as indicated. Statistical significance was determined by analysis of variance (ANOVA). (f) Oxygen consumption of male WT (n=5) and RIIβ KO mice (n=8) following vehicle or leptin i.c.v. injection. (g–j) Body weight-matched (g) WT (20.7±0.4 g, 4-week-old, n=9) and RIIβ KO (21.2±0.4 g, 6-week-old, n=8) male mice were selected for leptin injections. (h) Changes in daily food intake and (i) body weight of WT and RIIβ KO mice over 8 days following vehicle or leptin i.p. injections as indicated. (j) Fat pads weight and serum leptin levels were collected and assessed after the experiments. Data are expressed as mean±s.e.m. Two-way ANOVA was used for the effect of genotypes followed by Bonferroni’s post hoc tests or Student’s t-tests (*P<0.05, **P<0.01, ***P<0.001). NS, not significant.