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. 2011 Jul 11;121(8):3331–3342. doi: 10.1172/JCI44564

Figure 7. ERs suppress lipid synthesis via STAT3.

Figure 7

(A and B) INS-1 cells were treated with E2 for up to 2 hours (A) or with leptin, E2, PPT, G1, DPN, or EDC for 10 minutes (B), and phosphorylation of STAT3 was determined by Western blotting. Blots are representative of at least 3 experiments. (C) Immunofluorescent labeling of phosphorylated STAT3 (red) and DAPI (blue) in INS-1 cells treated with leptin, E2, PPT, G1, DPN, or EDC for 10 minutes. Images are representative of 2 experiments. Original magnification, ×100. (D) Cultured islets from the indicated mice were treated with E2 for 10 minutes, and STAT3 phosphorylation was determined by Western blotting. (E) Gene expression of Fasn, normalized to Actb, in control and PStat3–/– mouse islets treated with 6 μg/d E2 for 2 days (n = 11–20). (F) FAS enzymatic activity in islets of E2-treated control and PStat3–/– mice (n = 8–20). (G) TG content in islets of E2-treated control and PStat3–/– mice (n = 13–22). Data in E–G are from at least 3 experiments. *P < 0.05. (H) Proposed mechanism for ER-mediated inhibition of islet FA synthesis and lipid accumulation. Left: Lipid accumulation in islets leads to β cell failure. Right: ER activation suppresses FAS expression and activity, thus preventing lipid accumulation and protecting against β cell failure in a STAT3-dependent manner.