Enhanced PIP₃ signaling in POMC neurons causes K_ATP channel activation and leads to diet-sensitive obesity
J. Clin. Invest. Leona Plum, et al. 116:1886 doi:10.1172/JCI27123 [Go to this article.]

Figure 6
Hypothalamic neuropeptide expression and assessment of leptin sensitivity in control (white bars) and PPKO (black bars) mice. (A)Neuropeptide expression HFD-fed female mice at 6 and 20 weeks of age (n = 7–9 per group). CART, cocaine- and amphetamine-regulated transcript; AgRP, agouti-related peptide; TRH, thyrotropin-releasing hormone; CRH, corticotropin-releasing hormone. (B and C)Changes in food intake after intraperitoneal leptin treatment in ND-fed males at 15 weeks of age (B) and HFD-fed females at 10 weeks of age (C). Data represent daily food intake after a 3-day treatment with twice-daily injections of saline (–) or 2 mg/kg leptin (+; n = 4–6 per group). (D)Representative immunohistochemistry of pStat3 formation in hypothalamic neurons of male ND-fed control and PPKO mice at 12–15 weeks of age. Double immunohistochemistry of ARC neurons of CO_Arte1 and PPKO_Arte1 reporter mice was performed in ad libitum–fed mice, which were intravenously injected with either saline or leptin and sacrificed 30 minutes after the injection. Red, β-gal (POMC neurons); green, pStat3. Scale bar: 100 μm. (E)Quantification of pStat3-positive POMC neurons in hypothalamic slices of male CO_Arte1 and PPKO_Arte1 reporter mice on ND at the age of 12–15 weeks before (n = 1) and after (n = 3–8) leptin application (P > 0.05). Values are mean ± SEM. *P ≤ 0.05.