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 2
Unaltered regulation of the hypothalamo-pituitary-adrenal axis in PPKO mice. (A)Cre-mediated β-gal expression in a double-heterozygous reporter mouse (PomcCre-RosaArte1) in the ARC of the hypothalamus (H) and the anterior pituitary (P). No β-gal expression was observed in the adrenal gland (AG). (B)Representative H&E stain of the pituitary and the adrenal gland of a male control and a male PPKO mouse at the age of 12 weeks showed unaltered histomorphology of these organs in PPKO mice. (C)POMC mRNA expression in pituitary, hypothalamus, and adrenal gland of PPKO (black bars) and control (white bars) females on HFD at 12 weeks of age showed unaltered pituitary POMC expression in PPKO mice. Values are mean ± SEM (n = 6 per genotype). (D)Basal serum corticosterone levels at 12 weeks in PPKO (black bars) and control (white bars) HFD-fed females (left panel). Basal and stress-induced serum corticosterone levels at 12 weeks in PPKO and control SD males (right panel). Values are mean ± SEM (n = 6 per genotype). ***P ≤ 0.001 versus basal. Magnification, ×100.