Fig. 2: Deficiency of IL18r and NCC aggravates obesity, insulin resistance and inflammation in mice fed a HFD. | Nature Communications

Fig. 2: Deficiency of IL18r and NCC aggravates obesity, insulin resistance and inflammation in mice fed a HFD.

From: Differential IL18 signaling via IL18 receptor and Na-Cl co-transporter discriminating thermogenesis and glucose metabolism regulation

Fig. 2

a–d Bodyweight gain, glucose tolerance test (GTT), AUC of GTT, insulin tolerance test (ITT), AUC of ITT (WT: n = 10; Ncc−/−: n = 11, Il18r−/−: n = 11; Il18r−/−Ncc−/−: n = 11) (a), EAT, SAT, BAT, and liver weights (WT: n = 9; Ncc−/−: n = 14, Il18r−/−: n = 13; Il18r−/−Ncc−/−: n = 11) (b), energy intake (WT: n = 12; Ncc−/−: n = 11, Il18r−/−: n = 10; Il18r−/−Ncc−/−: n = 10) (c), and plasma insulin (WT: n = 11; Ncc−/−: n = 10, Il18r−/−: n = 13; Il18r−/−Ncc−/−: n = 8) and leptin (WT: n = 12; Ncc−/−: n = 15, Il18r−/−: n = 10; Il18r−/−Ncc−/−: n = 14) levels (d) from HFD-fed WT, Ncc−/−, Il18r−/−, and Il18r−/−Ncc−/− mice for 12 weeks. e–g Mouse metabolic parameters, including oxygen consumption (VO2) (e), carbon dioxide production (VCO2) (f), and energy expenditure (g) and their average values from full day cycle, light cycle, and dark cycle during 48 hrs of monitoring in WT, Ncc−/−, Il18r−/−, and Il18r−/−Ncc−/− mice (WT: n = 5; Ncc−/−: n = 6, Il18r−/−: n = 6; Il18r−/−Ncc−/−: n = 6). h Representative images of hematoxylin and eosin (H&E) staining and adipocyte sizes in EAT, SAT, and BAT from indicated mouse groups (WT: n = 14; Ncc−/−: n = 15, Il18r−/−: n = 9; Il18r−/−Ncc−/−: n = 12); scale bar: 50 μm. i. Plasma IL1β (WT: n = 6; Ncc−/−: n = 4, Il18r−/−: n = 4; Il18r−/−Ncc−/−: n = 7), IL6 (WT: n = 9; Ncc−/−: n = 12, Il18r−/−: n = 7; Il18r−/−Ncc−/−: n = 9), MCP1 (WT: n = 8; Ncc−/−: n = 12, Il18r−/−: n = 13; Il18r−/−Ncc−/−: n = 9), IFN-γ (WT: n = 10; Ncc−/−: n = 16, Il18r−/−: n = 12; Il18r−/−Ncc−/−: n = 14), and TNF-α (WT: n = 6; Ncc−/−: n = 4, Il18r−/−: n = 6; Il18r−/−Ncc−/−: n = 4) levels from indicated mouse groups. j Mac-3 immunostaining of representative EAT sections and quantification from indicated mouse groups (WT: n = 11; Ncc−/−: n = 12, Il18r−/−: n = 17; Il18r−/−Ncc−/−: n = 12); scale: 50 μm. Data are mean ± SEM, two-way ANOVA repeated-measures (a) or one-way ANOVA test (b-j), followed by LSD post-test. Sample sizes were all biologically independent samples.

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