Gut Microbiota Is a Key Modulator of Insulin Resistance in TLR 2 Knockout Mice (original) (raw)
Figure 4
Evaluation of pathways involved in the impairment of insulin signaling.
Phosphorylation of JNK in muscle (A), liver (B), and white adipose tissue (WAT) (C). Phosphorylation of PERK in muscle (D), liver (E), and WAT (F). Serine 307 phosphorylation of IRS-1 from muscle (G), liver (H), and WAT (I). Activation of TLR4 (studied by the immunoprecipitation of MyD88 and blotting with TLR4) in muscle (J), liver (K), and WAT (L). JNK, PERK, and IRS-1 protein expression in muscle, liver, and white adipose tissue (A–I, lower panels). Expression of IκB-α in muscle (M), liver (N), and WAT (O). Equal protein loading in the gel was confirmed by reblotting the membrane with an anti-β-actin antibody (M–O, lower panels). NFκB activation in muscle (P), liver (Q), and WAT (R). All evaluations were made with mice on standard chow. Data are presented as means ± S.E.M from six to eight mice per group from experiments that were repeated at least three times. * p<0.05 between TLR2−/− mice and their controls.