Possible involvement of PI3K-dependent pathways in the increased VEGF120 release from osteoblastic cells preloaded with palmitate in vitro

•The palmitate-preloaded cells showed the significant increase of VEGF120 release.•The palmitate-induced increase of VEGF120 release from UMR-106 cells may be mediated through, at least partly, TLR4.•The palmitate may increase the expression and secretion of VEGF120 through, mainly, the PI3K pathways in UMR-106 cells. It have been reported that abnormal bone metabolism often occurs in patients with type 2 diabetes, but the underlying mechanisms remain to be elucidated. In recent years dyslipidemia (hyperlipidemia) has been presumed to have an influence on bone metabolism. In addition, the involvements of VEGF and MCP-1 derived from osteoblasts in bone abnormal metabolism were also observed. Thus, we investigated the pathogenic mechanism of this abnormal bone metabolism, which is included in the regulation of VEGF and MCP-1 secretions from osteoblasts, by using UMR-106 osteosarcoma cells as an osteoblast cell model and treating them with palmitate in order to mimic a state of hyperlipidemia. Palmitate-preloaded cells showed the significant increase of VEGF120 release (1.8-fold vs. control cells, p