Artemisia scoparia promotes adipogenesis in the absence of adipogenic effectors

Abstract Objective Extracts of Artemisia scoparia (SCO) have antidiabetic properties in mice and enhance adipogenesis in vitro , but the underlying mechanisms are unknown. Thiazolidinediones, including rosiglitazone (ROSI), are pharmacological activators of peroxisome proliferator‐activated receptor gamma that also promote adipogenesis. The aim of this study was to examine adipogenic pathways responsible for SCO‐mediated adipogenesis and identify potential differences between SCO and ROSI in the ability to promote adipocyte development. Methods The ability of SCO or ROSI to promote adipogenesis in 3T3‐L1 cells following systematic omission of the common triad of adipogenic effectors dexamethasone, 1‐methyl‐3‐isobutylxanthine (MIX), and insulin was examined. Adipogenesis was assessed by both neutral lipid quantitation and adipocyte marker gene expression. Results The results demonstrate that SCO and ROSI promote adipogenesis and increase the expression of several peroxisome proliferator‐activated receptor gamma target genes involved in lipid accumulation in the absence of MIX. However, ROSI can enhance adipogenesis in the absence of MIX and insulin and differentially regulates adipogenic and lipid metabolism genes as compared with SCO. Conclusions These data demonstrate the adipogenic capabilities of SCO are similar but not identical to ROSI, thereby warranting further research into SCO as a promising source of therapeutic compounds in the treatment of metabolic disease states.