FIG. 2.

Socs3 overexpression in POMC neurons leads to increased body weight and adiposity, decreased resting energy expenditure, and resistance to leptin's anorexigenic effects. A: Body weight of POMC-Socs3-OE on chow diet at indicated ages. Mutants became significantly heavier at 15 weeks of age (controls n = 9–13, mutants n = 7–10). B: Analysis of lean mass and fat mass by DEXA of POMC-Socs3-OE at 8 and 25 weeks of age (controls n = 10, mutants n = 8). (C) Plasma leptin levels under fed conditions for 25-week-old POMC-Socs3-OE mice were significantly higher (controls n = 9, mutants n = 8). D: A 24-h food intake was measured in 8-week-old controls and POMC-Socs3-OE mutant mice (controls n = 11, mutants n = 7). E and F: Oxygen consumption was measured in 8-week-old mice, and the values were normalized to lean body mass of each mouse. Daytime: 1100–1700; nighttime: 1900–0700. A representative trace is shown in F. G: The 9-week-old POMC-Socs3-OE and control mice were injected intraperitoneally with saline twice daily for 3 consecutive days and leptin (2.5 mg/kg) twice on the fourth day. A 24-h food intake after leptin treatment was reported as a ratio of food intake after saline treatment (controls n = 11, mutants n = 7). Data represent mean ± SEM. *P < 0.05, **P < 0.01, between controls and mutants as determined by 2-way ANOVA using litters and genotypes as variables. ns, nonsignificant.