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. 2016 Nov 17;6:37323. doi: 10.1038/srep37323

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Copyright © 2016, The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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(A) PPARγ transactivation assay with 10 μM doses of compounds 3a–3 g, 4, PODO-1, and pioglitazone. *P < 0.05 and **P < 0.01 versus the PODO-1 group; ^##P < 0.001 versus the pioglitazone group. (B) Representative concentration-response curves of reporter gene transactivation by compound 3a, compound 3f, and PODO-1 compared with pioglitazone. (C) Insulin-resistant cells were incubated with 20 μM doses of the PODO-1 derivatives and pioglitazone. *P < 0.05 and **P < 0.01 versus the insulin-resistant control; ^#P < 0.05 versus the normal control. (D) Comparative assessment of the glucose uptake potential of compound 3a, compound 3f, and pioglitazone in the insulin-resistant model of HepG2 cells. The standard error bars represent 3 independent experiments, with each experiment performed in triplicate.