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. 2024 May 30;15:4605. doi: 10.1038/s41467-024-48220-5

Fig. 1. IRF3 mediates insulin resistance in response to TLR4 ligands in cultured adipocytes.

Fig. 1

a Glucose uptake in mouse adipocytes after treatment with varying doses of LPS for 2 days (n = 8). b Western blot showing phosphorylation of murine IRF3 (S388) in mouse adipocytes after 30 min of LPS (700 ng/ml) treatment. c Glucose uptake in mouse adipocytes transduced with lentivirus expressing shRNA against Irf3 or shScr control hairpin in the absence or presence of LPS (700 ng/ml) (n = 8). d Western blot of pAKT (S473) and IRF3, e Glucose uptake (n = 6) in WT and FI3KO SVF-derived adipocytes treated with control or 100 nM insulin. f Glucose uptake in human SGBS adipocytes after treatment with varying doses of LPS for 2 days (n = 8). g Western blot showing phosphorylation of human IRF3 (S396) in human SGBS adipocytes after 30 mins of LPS (700 ng/ml) treatment. h Western blot of pAKT (S473) and IRF3 in human SGBS adipocytes transduced with lentivirus expressing shRNA against Irf3 or a scrambled control hairpin (shScr). i Glucose uptake in human SGBS adipocytes transduced with lentivirus expressing shRNA against Irf3 or shScr control hairpin in the absence or presence of LPS (700 ng/ml) (n = 8). Statistical significance was assessed by three-way ANOVA (c and i) or two-way ANOVA (a, d, e, f, and h). Data are expressed as mean ± SEM.