Sclerostin (SOST), a protein secreted from mature osteocytes in response to mechanical unloading and other stimuli, inhibits the osteogenic Wnt/β-catenin pathway in mesenchymal stem cells (MSCs) impeding their ability to differentiate into mineralizing osteoblasts.
Purpose: This review summarizes the crosstalk between adipose tissue and bone. It also reviews the origin, regulation, and role of SOST in osteogenesis and brings attention to an emerging role of this protein in the regulation of adipogenesis.
Recent findings: Bone-derived molecules that drive MSC adipogenesis have not previously been identified, but recent findings suggest that SOST signaling may induce adipogenesis. In vivo SOST acts locally to induce changes in bone and, in vitro, increases adipogenesis in 3T3-L1 preadipocytes.
Summary: SOST is able to induce adipogenesis in certain preadipocytes, however bone-specific studies are needed to determine the effect of local SOST concentrations in healthy and disease models on bone marrow adipose tissue.
Keywords: Adipogenesis; Bone Marrow Adipose Tissue; Fat; LRP; Sclerostin; Wnt.