Effect of PTP1B deficiency on hypothalamic AMPK activity and neuropeptide expression. Panels A to C show data from whole-body PTP1B−/− mice, and panel D shows data from neuronal PTP1B−/− mice. (A) α1 and α2 AMPK activities in ARC, PVN, VMH/DMH, and LH of whole-body PTP1B−/− mice in the fed state. (B) POMC expression in hypothalamus of fasted mice injected with saline or leptin (intraperitoneally). (C) NPY and AgRP mRNA expression in hypothalamus of fasted and fed mice and MCH mRNA expression in hypothalamus of fed mice. (D) α2 AMPK activity in ARC and PVN hypothalamus of neuronal PTP1B−/− mice in the fed state. All experiments were carried out using 12-week-old (A) or 8- to 10-week-old (B to D) male WT and whole-body (A to C) or neuronal (D) PTP1B−/− mice on a chow diet. For panel A, n = 6 to 8 for each genotype; panels B and C, n = 12 per genotype; and panel D, n = 11 to 12 per genotype. Data are expressed as means ± SEM. *, P < 0.05 compared to results for WT mice.