The neural cell adhesion molecule (NCAM) participates in the adipogenesis of murine bone marrow stromal cells via the insulin signaling pathway.

Abstract

Cell adhesion molecules have long been thought to play an important role in the complex process of adipogenesis. However, little information has been uncovered on the molecular basis of their functions in adipogenesis. The neural cell adhesion molecule (NCAM), a member of the immunoglobulin superfamily of cell adhesion molecules, was found to play a role in the adipogenesis of murine bone marrow stromal cells (BMSCs). Therefore, the objective of this study is to investigate the molecular mechanisms of how NCAM participates in adipogenesis. Our results show that NCAM-deficient cells possess decreased levels of activated Akt and ERK1/2. While both molecules were found to play important roles in adipogenesis, the inhibition of Akt alone could result in a complete blockade of adipogenesis in BMSCs, indicating its importance in the adipocyte differentiation process. We discovered that the decreased levels of Akt observed in NCAM-deficient mice were due a defect in the insulin signaling pathway, more specifically, at the level of the insulin receptor itself. All in all, our results indicate a role for NCAM in the insulin signaling pathway, one of the major pathways leading to adipogenesis.