Estrogen suppresses adipogenesis by inhibiting S100A16 expression
- Rihua Zhang2,*,
- Dongming Su3,*,
- Weidong Zhu4,*,
- Qiong Huang1,
- Menglan Liu1,
- Yi Xue6,
- Yuanyuan Zhang1,
- Dong li5,
- Allan Zhao3 and
- Yun Liu1⇑
- 1Department of Geratology
2Laboratory Animal Center, The First Affiliated Hospital
3The Center of Metabolism, Nanjing Medical University, Nanjing 210029, China
4Department of Urology, Zhongda Hospital Affiliated to Southeast University, Nanjing 210008, China
5Department of Orthopedics, Jiangsu Province Hospital of TCM, Affiliated Hospital of Nanjing University of TCM, Nanjing, Jiangsu, China
6Department of Endocrinology, Changzhou Wujin People's Hospital, 213000 Changzhou, Jiangsu, China
- Correspondence should be addressed to Y Liu; Email: liuyun{at}njmu.edu.cn
Abstract
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 PPARγ, aP2, C/EBPα, 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.
- Revision received 31 January 2014
- Accepted 5 February 2014
- Made available online as an Accepted Preprint 5 February 2014
- © 2014 The authors
This work is licensed under a Creative Commons Attribution 3.0 Unported License
