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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 7. — Differential response of PPARγ1 KO and PPARγ2 KO mice to antidiabetic drug treatment. (A) Scheme of experiment design of HFD and rosiglitazone treatment. (B,I) Intraperitoneal glucose tolerance test of PPARγ1 KO (B) and PPARγ2 KO (I) mice after 6 wk of rosiglitazone treatment or vehicle treatment. n = 5 per group. (C,J) Intraperitoneal glucose tolerance test of PPARγ1 KO (C) and PPARγ2 KO (J) mice and their control littermates after 6 wk of rosiglitazone treatment. n = 5–7 per group. (D,K) Body weights from PPARγ1 KO (D) and PPARγ2 KO (K) mice and their control littermates after 6 wk of rosiglitazone treatment. n = 5–7 per group. (E,L) Body weight gain of PPARγ1 KO (E) and PPARγ2 KO (L) mice and their control littermates after 6 wk of rosiglitazone treatment. n = 5–7 per group. (F–H) iWAT (F), eWAT (G), and BAT (H) weights from PPARγ1 KO mice and their control littermates after 6 wk of rosiglitazone treatment. n = 5–6 per group. (M–O) iWAT (M), eWAT (N), and BAT (O) weights from PPARγ2 KO mice and their control littermates after 6 wk of rosiglitazone treatment. n = 5–7 per group. Data are expressed as mean ± SEM. (*) P < 0.05, (ns) not significant; Student's t-test for D–H and K–O. (*) P < 0.05, (**) P < 0.01, (****) P < 0.0001; two-way ANOVA for B, C, I, and J.