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. 2019 Mar 5;16:17. doi: 10.1186/s12986-019-0344-9

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 8 — Effects of PPARγ agonist and antagonist on CMKLR1 level in the livers (a) and gastrocnemius (b) of EDM rats. The exercise-induced decreases of CMKLR1 in the livers (a) and gastrocnemius (b) of EDM rats were reversed by PPARγ antagonist GW9662 at protein levels. PPARγ agonist pioglitazone further strengthened the reduction of CMKLR1 in the gastrocnemius (b) instead of the livers (a) of EDM rats. The blots of CMKLR1 were quantified by Tanon software and normalized against β-actin or GAPDH, then the normalized numbers were compared between different groups (bottom). DM: diabetes mellitus; EDM: exercised DM; EDP: EDM + pioglitazone; EDG: EDM + GW9662. ^*P<0.05, ^**P<0.01 vs DM. ^#P<0.05, ^##P<0.01 vs EDM