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. 2022 Mar 1;36(5-6):300–312. doi: 10.1101/gad.349232.121

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© 2022 Hu et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — Metabolic phenotypes of PPARγ1 KO and PPARγ2 KO mice under HFD treatment. (A,D) Body weight gain of PPARγ1 KO (A) and PPARγ2 KO (D) mice and their control littermates on HFD. n = 5–13 per group. (B,E) iWAT, eWAT, and BAT weights from PPARγ1 KO (B) and PPARγ2 KO (E) mice and their control littermates after 12 wk of HFD. n = 5–13 per group. (C,F) Intraperitoneal glucose tolerance test of PPARγ1 KO (C) and PPARγ2 KO (F) mice and their control littermates under 12-wk HFD treatment. n = 5–13 per group. Data are expressed as mean ± SEM. (*) P < 0.05, (**) P < 0.01, (ns) not significant; Student's t-test.