GPR26 deficiency stimulates AMPK phosphorylatoin in the hypothalamus.

<p>After 12-weeks of high-fat diet, GPR26 knockout mice (KO) and wild type littermates (WT) were fasted overnight and tissues samples were collected. Western blot analysis was carried out to determine the effect of GPR26 deficiency on phosphorylation of AMPK at Ser172, a key activation site in hypothalamus (<b>A</b>) and liver (<b>B</b>). (<b>C–D</b>), quantitative analysis of AMPK phosphorylation in panel A and B, respectively. N = 4, <i>*p<0.05</i>, **<i>p</i><0.01 when compared with wild type controls.