Figure 2. Absence of leptin signaling in early life alters the energy balance and predisposes the animals to obesity.

(A–D) Body weight (n = 13–22), body adiposity (S.C., subcutaneous; P.G., perigonadal; R.P., retroperitoneal fat pads; n = 10–25), serum leptin concentration (n = 9–25) and food intake (n = 13–22) in male mice treated with tamoxifen at 10 weeks of age. (E–F) Energy expenditure (VO₂) during dark phase, light phase and 24 hr in male mice (n = 9–15). (G–H) Respiratory exchange ratio (RER) in male mice (n = 9–15). (I–J) Voluntary ambulatory activity in male mice (n = 9–15). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001 (Figure 2—source data 1).

Figure 2—figure supplement 1. LepR reactivation in adult females does not restore completely the energy homeostasis.

(A–D) Body weight (n = 9–33), body adiposity (S.C., subcutaneous; P.G., perigonadal; Ov., ovarian; R.P., retroperitoneal fat pads; n = 8–45), serum leptin concentration (n = 8–26) and food intake (n = 8–30) in female mice treated with tamoxifen at 10 weeks of age. (E–F) Energy expenditure (VO₂) during dark phase, light phase and 24 hr in female mice (n = 5–10). (G–H) Respiratory exchange ratio (RER) in female mice (n = 5–10). (I–J) Voluntary ambulatory activity in female mice (n = 4–12). *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001. Mean ±S.E.M (Figure 2—figure supplement 1—source data 1).