The aim of this study is to determine the effects of E2 on metabolic syndrome and the molecular mechanisms involving S100A16. Ovariectomized (OVX) rat models and mouse embryonic fibroblasts cell models were used. E2 loss in OVX rats induced body weight gain and central abdominal fat accumulation, which were ameliorated by E2 treatment under chow and high-fat diet (HFD) conditions. E2 decreased the expression of the adipocyte marker genes PPAR γ, aP2, C/EBP α, and S100A16. E2 inhibited adipogenesis. Overexpression of S100A16 reversed the E2-induced adipogenesis effect. A luciferase assay showed that E2 inhibited the expression of S100A16. E2 treatment decreased body weight gain and central abdominal fat accumulation under both chow and HFD conditions. Also, E2 suppressed adipogenesis by inhibiting S100A16 expression.
Estrogen suppresses adipogenesis by inhibiting S100A16 expression
Rihua Zhang,D. Su,Weidong Zhu,Qiong Huang,Menglan Liu,Yi-ping Xue,Yuanyuan Zhang,Dong Li,A. Zhao,Yun Liu
Published 2014 in Journal of Molecular Endocrinology
ABSTRACT
PUBLICATION RECORD
- Publication year
2014
- Venue
Journal of Molecular Endocrinology
- Publication date
2014-02-05
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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