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. 2014 Jul 1;20(1):41–53. doi: 10.1016/j.cmet.2014.03.031

Figure 7.

Figure 7

Effect of Physiological Levels of E2 and Pharmacological and Genetic Manipulation of ERα on the VMH AMPK-SNS-BAT Axis

(A–C) (A) Serum E2 levels (left panel) and core temperature (right panel), (B) protein levels (upper panel) and western blot autoradiographic images of BAT UCP1 protein (lower panel), and (C) western blot autoradiographic images (left panel) and levels of proteins of AMPK pathway in the VMH (right panel) of diestrus cycled rats.

(D–F) (D) Body weight change (left panel) and daily food intake (right panel), (E) protein levels (upper panel) and western blot autoradiographic images of BAT UCP1 protein (lower panel), and (F) western blot autoradiographic images (left panel) and levels of proteins of AMPK pathway in the VMH (right panel) of intact rats ICV treated with the specific ERα antagonist MPP.

(G–I) (G) Body weight change (left panel) and daily food intake (right panel), (H) protein levels (upper panel) and western blot autoradiographic images of BAT UCP1 protein (lower panel), and (I) western blot autoradiographic images (left panel) and levels of proteins of AMPK pathway in the VMH (right panel) of intact rats stereotaxically treated within the VMH with lentivirus encoding short hairpin RNA of the ERα. Error bars represent SEM; n = 7–8 animals per experimental group. ∗, ∗∗, and ∗∗∗p < 0.05, 0.01, and 0.001 versus OVX, vehicle ICV, or GFP VMH.