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. 2018 Oct 29;8:15973. doi: 10.1038/s41598-018-34238-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Summary of the pathways impacted by chronic BP3 treatment in liver and WAT in obese mouse models. BP3 enhances FGF/FGFR signaling and downstream activation of Akt and IL6/Stat3 that lead to the inhibition of gluconeogenesis, through Ppargc1a/G6pc downregulation. The parallel activation of Akt and Stat3 results in an inhibition of Ppargc1b and/or Srebf1, key regulators of downstream lipogenic enzymes, thus leading to the inhibition of de novo lipogenesis and TG synthesis.