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. 2017 Sep 6;7:10633. doi: 10.1038/s41598-017-10410-1

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© The Author(s) 2017

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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Inhibition of CBR1 in a murine model of diet-induced obesity results in increased GR activation and metabolic dysfunction. (A) Hepatic 20β-DHB levels were significantly lower in quercetin treated mice, (B) 20β-DHFB levels were not altered in subcutaneous adipose tissue, (C) plasma 20β-DHB levels were not altered by quercetin treatment (D) quercetin treatment resulted in increased peak plasma corticosterone levels. (E) Bodyweight was not different between mice in the vehicle treated group and mice treated with quercetin. (F,G) Quercetin-treated mice were significantly more insulin resistant and had higher fasted plasma insulin concentrations. (H) mRNA transcript levels of hepatic Per1 were increased in quercetin treated mice, (I) Adipose mRNA expression of Per1, Adiponectin (Adipq) and lipoprotein lipase (Lpl) were not altered by quercetin treatment. Data are mean ± SEM, n = 12/group, *P < 0.05.