The Chemokine CXCL16 Can Rescue the Defects in Insulin Signaling and Sensitivity Caused by Palmitate in C2C12 Myotubes

摘要: In obesity, macrophages infiltrate peripheral tissues and secrete pro-inflammatory cytokines that impact local insulin sensitivity. Lipopolysaccharide (LPS) the saturated fatty acid (FA) palmitate polarise towards a phenotype in vitro indirectly cause resistance (IR) myotubes. contrast, unsaturated FAs confer an anti-inflammatory counteract actions of palmitate. To explore paracrine mechanisms interest, J774 were exposed to ± palmitoleate or control medium conditioned media generated screened using cytokine array. Of 62 examined, 8 significantly differentially expressed following FA treatments. Notably, CXCL16 secretion was downregulated by follow-up experiments ELISAs, this downregulation confirmed reversed simultaneous addition oleate, while LPS also diminished secretion. dissect potential effects CXCL16, C2C12 myotubes treated with induce IR, recombinant soluble (sCXCL16), combined treatment, medium. Palmitate caused expected reduction insulin-stimulated Akt activation glycogen synthesis, whereas treatment sCXCL16 attenuated these effects. These data indicate putative role for preservation signaling context chronic low-grade inflammation skeletal muscle.