Estrogen suppresses adipogenesis by inhibiting S100A16 expression

The aim of this study is to determine the effects of E(2) on metabolic syndrome and the molecular mechanisms involving S100A16. Ovariectomized (OVX) rat models and mouse embryonic fibroblasts cell models were used. E(2) loss in OVX rats induced body weight gain and central abdominal fat accumulation, which were ameliorated by E(2) treatment under chow and high-fat diet (HFD) conditions. E(2) decreased the expression of the adipocyte marker genes PPAR γ, aP2, C/EBP α, and S100A16. E(2) inhibited adipogenesis. Overexpression of S100A16 reversed the E(2)-induced adipogenesis effect. A luciferase assay showed that E(2) inhibited the expression of S100A16. E(2) treatment decreased body weight gain and central abdominal fat accumulation under both chow and HFD conditions. Also, E(2) suppressed adipogenesis by inhibiting S100A16 expression.