Figure 3

LEP-deficiency induced obesity, glucose intolerance and hyperinsulinemia in Lep rats.

(A) Daily food intake (Means ± SD) for WT (n = 5) and Lep^{∆I14/∆I14} (n = 6) measured over 7–8 weeks. *P < 0.05 vs. controls. **P < 0.01 vs. controls. ***P < 0.001 vs. controls. (B) Body weight was measured over 9 weeks for WT (n = 5) and Lep^{∆I14/∆I14} males (n = 6) and WT (n = 6) and Lep^{∆I14/∆I14} females (n = 6). *P < 0.01 vs. controls. **P < 0.01 vs. controls. ***P < 0.001 vs. controls. (C) Serum INSULIN level in 8-wk-old male WT (n = 4) and Lep^{∆I14/∆I14} rats (n = 5) and female WT (n = 4) and Lep^{∆I14/∆I14} rats (n = 6). ***P < 0.001 vs. controls. (D) Male WT (n = 5) and Lep^{∆I14/∆I14} rats (n = 6) at age of wk-16 were ip injected with D-glucose and serum glucose levels were determined at 0, 30, 60, 90 and 120 min after administration. *P < 0.05 vs. controls. (E) Hyperphagia and obesity were rescued by subcutaneous infusion of recombinant LEP. Two individual female Lep^{∆I14/∆I14} rats were treated with rat recombinant Lep via subcutaneous implantation of an Alzet osmotic minipump (200 μg/kg/day) for 7 days before switching LEP to saline, while the WT female controls (n = 3) were implanted with a saline-filled minipump. For Lep^{∆I14/∆I14} rats, solid arrow indicates the start of LEP treatment; solid arrowhead indicates the switch of LEP to saline. For WT controls, open arrow indicates the start of minipump implantation; open arrowhead indicates withdrawal of minipump. Numbers near each body-weight point are the daily food intake (g) measured on the same day.