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. 2021 Dec 4;12(2):11784–11796. doi: 10.1080/21655979.2021.1996508

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© 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — RANKL inhibited the effects of BBR+Rb1 on adipogenesis and insulin resistance in TNF-α-treated adipocytes. (a) Adipogenesis was evaluated by performing oil red O staining assay (**, p < 0.01, compared to Control; ##, p < 0.01, compared to TNF-α; &&, p < 0.05, compared to BBR+Rb1). (b) The gene and protein expression levels of PPAR-γ, C/EBPα, and SREBP-1 c were measured in RT-PCR and western blot assays, respectively (**, p < 0.01, compared to Control; ##, p < 0.01, compared to TNF-α; &&, p < 0.05, compared to BBR+Rb1). (c) The gene and protein expression levels of IRS-1 and GLUT4 were measured in RT-PCR and western blot assays, respectively (**, p < 0.01, compared to Control; ##, p < 0.01, compared to TNF-α; &&, p < 0.01, compared to BBR+Rb1)