Figure 3.

Reactivation of Pomc expression in the arcuate nucleus or MTII treatment reduced plasma adiponectin. (A) Schematic representation of the generation of transgenic mice with Cre recombinase-inducible activation of Pomc gene expression in the arcuate nucleus after tamoxifen injection. The inducible ArcPomc^−/− transgenic mice had a loxP-flanked neomycin (neo) resistance cassette inserted upstream of the deleted neuronal Pomc enhancer 2 (nPE2∗) in the Pomc gene. Purple oval, neuronal Pomc enhancer 1 (nPE1); yellow oval, Pomc promoter; and green boxes, Pomc exons. (B) Serial body weights of 41- to 55-week-old female mice at the indicated time points after tamoxifen injection (n = 5–7). (C) Tissue weight 53 days post-tamoxifen injection (n = 5–7). (D) Plasma adiponectin before and after Pomc gene activation in Arc (n = 5–7). (E) Immunoblots of plasma protein from female inducible ArcPomc^−/− and Pomc^+/+ mice pre- and post-activation of Pomc expression in Arc (n = 4). (F) Relative total and high molecular weight adiponectin band intensities (n = 4). (G) Plasma adiponectin levels after melanotan II administration (n = 7, 13–17 weeks old, female). Values were normalized to saline injection within genotypes at respective time points. Two-way ANOVAs with post hoc Bonferroni's and Tukey's multiple comparisons were conducted to examine the genotype and tamoxifen treatment effects. Two-tailed unpaired nonparametric Mann–Whitney tests were used for comparisons of tissue weights. Data shown are the mean ± s.e.m of biologically independent samples. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001.