Figure 4.

Oncostatin-M is acutely induced by exercise and increases basal lipolysis in human adipocytes

(A–D) Gene expression of candidate secreted factors oncostatin-M, GDF15, SFRP4, and MXRA5 selected for further validation.

(E) Human adipocytes were treated with recombinant proteins for 1 h, and kinase activity was assessed using serine-threonine substrate array (n = 5).

(F–I) Kinase activity in response to oncostatin-M, GDF15, SFRP4, and MXRA5 was predicted by computational analysis of differentially phosphorylated peptide signatures. The kinase statistic parameter reflects the change in kinase activity, whereas the specificity parameter indicates how specific the peptide signature is to a particular kinase.

(J) Protein-protein interaction (PPI) network and reactome pathway analysis of differentially active kinases. Kinase score reflects kinase activation in response to oncostatin-M compared to control cells, and the node degree is a measure of how connected each node is within the network.

(K) PPI network and reactome pathway analysis of differentially active kinases. Kinase score reflects kinase activation in response to SFRP4 compared to control cells, and the node degree is a measure of how connected each node is within the network.

(L–N) Western-blot quantification and representative image of P-STAT3 Y705, P-ERK1/2 T202/Y204, and P-HSL S563 after 1 h incubation with recombinant proteins in isolated human adipocytes (one-way ANOVA) (n = 5).

(O) Lipolysis assay in control, 1 μM, and 10 μM isoprenaline conditions (two-way ANOVA). ∗∗∗∗p < 0,0001; ∗∗∗p < 0.001; ∗∗p < 0,01; ∗p < 0,05.

Error bars show SEM.