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. 2022 Dec 8;13:7582. doi: 10.1038/s41467-022-35256-8

Fig. 9. Adipocyte-selective depletion of IL18r impairs white adipocyte glucose metabolism and insulin signaling and exacerbates obesity and insulin resistance.

Fig. 9

ac Bodyweight gain (Il18rfl/fl: n = 8; Il18rfl/flAdipoqCre: n = 9), GTT and AUC of GTT (n = 8 per group), ITT and AUC of ITT (n = 8 per group) (a), EAT, SAT, BAT, and liver weight (Il18rfl/fl: n = 8; Il18rfl/flAdipoqCre: n = 9) (b), and energy intake (n = 7~8 each) (Il18rfl/fl: n = 7; Il18rfl/flAdipoqCre: : n = 9) (c) in Il18rfl/fl and Il18rfl/flAdipoqCre fed a HFD for 12 weeks. d H&E of EAT, SAT, and BAT from indicated groups of mice (Il18rfl/fl-EAT: n = 9; Il18rfl/flAdipoqCre-EAT: n = 9; Il18rfl/fl-SAT: n = 12; Il18rfl/flAdipoqCre-SAT: n = 9; Il18rfl/fl-BAT: n = 11; Il18rfl/flAdipoqCre-BAT: n = 8). Scale: 50 μm. Inset: 25 μm. ef RT-PCR analysis of lipogenic, lipolytic, glucose metabolic, thermogenic, and inflammatory genes in EAT (e) and SAT (f) from indicated mice (Il18rfl/fl: n = 10; Il18rfl/flAdipoqCre: n = 9). g Immunoblots of pAKT, AKT, and GAPDH and quantification of pAKT/AKT in WAT from indicated mice (n = 6 per group). h-i. Representative FACS images and quantification of CD11b+Siglec F+ eosinophils (Il18rfl/fl-EAT: n = 8; Il18rfl/flAdipoqCre-EAT: n = 6; Il18rfl/fl-SAT: n = 9; Il18rfl/flAdipoqCre-SAT: n = 6; Il18rfl/fl-BAT: n = 4; Il18rfl/flAdipoqCre-BAT: n = 4) (h) and CD11b+F4/80 + total, CD11b+F4/80 +CD11c+ M1, and CD11b+F4/80 +CD206+ M2 macrophages in EAT, SAT, and BAT (Il18rfl/fl-EAT: n = 6; Il18rfl/flAdipoqCre-EAT: n = 6; Il18rfl/fl-SAT: n = 7; Il18rfl/flAdipoqCre-SAT: n = 6; Il18rfl/fl-BAT: n = 4; Il18rfl/flAdipoqCre-BAT: n = 3) (i) from indicated mice. Data are mean ± SEM, two-way ANOVA repeated-measures, followed by LSD post-test (a), two-sided Student’s t-test (bd, h) and two-sided Mann-Whitney U test (g). Sample sizes were all biologically independent samples.