Enhanced PIP3
signaling in POMC neurons causes KATP
channel activation and leads to diet-sensitive obesity
J. Clin. Invest. Leona Plum, et al. 116:1886 doi:10.1172/JCI27123 [
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Figure 4Phenotypic characteristics of control (open symbols; white bars) and PPKO (filled symbols; black bars) female mice under different dietary conditions with respect to energy homeostasis. (
A)Average body weight of ND- (triangles) and HFD-fed (circles) female mice (
n = 6–81). (
B)Outward appearance of 2 control and 2 PPKO female mice of the same litter at the age of 20 weeks (17 weeks of HFD feeding). (
C)Exemplary demonstration of parametrial fat pads in situ (upper panel; black diamonds) and ex situ (lower panel; white diamonds) of control and PPKO females at the age of 20 weeks. (
D)Absolute parametrial fat pad weights of female control and PPKO mice on ND and HFD (
n = 3–17) and relative (corrected for body weight) parametrial fat pad weights of female HFD-fed control and PPKO mice. (
E)Serum leptin levels of female control and PPKO mice on ND and HFD (
n = 4–30). (
F)Daily caloric intake of female control and PPKO mice on HFD at the age of 10–13 weeks (
n = 4–6). (
G)Oxygen consumption of female mice on HFD at the age of 12 weeks (
n = 7–8). (
H)Locomotor activity of female mice on HFD at the age of 12 weeks (
n = 7–8). Unless otherwise indicated, data were collected at 20 weeks of age. Values are mean ± SEM. *
P ≤ 0.05, **
P ≤ 0.01, ***
P ≤ 0.001 versus control.