Fig 2: TGF-β and PDGF promote IL-6 release by activated fibroblasts on transwell. Variation of IL-6 release from NIH-3T3 fibroblasts, cultured on the upper side of transwell, at the end of 5 days exposure to TGF-β (5 ng/mL), in the absence or presence of 10 μM TGF-β receptor inhibitor (SB431542), or to PDGF (50 ng/mL) in the absence or presence of 1 μM of the PDGFRα/β inhibitor (CP-673451) (a), or to 4T1 cells in the absence or presence of the same inhibitors and of SMAD3 inhibitor (SIS3) (b). Untreated 3T3 cells in monoculture have been considered as reference (1). Data, represented as box-and-whisker plots, were compared by One-way ANOVA (**** p < 0.0005, *** p < 0.001, ** p < 0.01, * p < 0.05; n = 4–14).

Fig 3: The effects of IL-6 on adipose tissue lipolysis.Short term (2 hours) IL-6 (150 ng/ml) treatment does not increase A) glycerol or B) fatty acid release from cultured epididymal mouse adipose tissue. Epinephrine (2 hours, 1 μM) treated cultures were included as a positive control. Data are presented as means + SE for 7 cultures per group. * P<0.05 compared to vehicle and IL-6 groups.

Fig 4: Beta adrenergic signalling in adipose tissue from WT and IL-6−/− mice.Exercise-induced increases in A) CREB and B) HSL phosphorylation are not different in eWAT from WT and IL-6−/− mice. Epinephrine stimulated C) glycerol and D) fatty acid release are not different in eWAT from either WT or IL-6−/− mice. Data are presented as means + SE for 6–12 samples/animals per group. * P<0.05 compared to sedentary control group in A and B or vehicle treated control group in C and D.

Fig 5: IL-6 signalling in cultured adipose tissue. Ex vivo IL-6 treatment (150 ng/ml, 30mins) increases the phosphorylation of STAT3, AMPK and ACC but not the p38MAPK signalling pathways in cultured eWAT. Data are presented as means + SE for 7 cultures per group. Representative Western blot images are given to the right of the quantified data. * P<0.05 versus vehicle control.