title: Estrogen suppresses adipogenesis by inhibiting S100A16 expression.
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.
authors: Department of Geratology Laboratory Animal Center, The First Affiliated Hospital The Center of Metabolism, Nanjing Medical University, Nanjing 210029, China Department of Urology, Zhongda Hospital Affiliated to Southeast University, Nanjing 210008, China Department of Orthopedics, Jiangsu Province Hospital of TCM, Affiliated Hospital of Nanjing University of TCM, Nanjing, Jiangsu, China Department of Endocrinology, Changzhou Wujin People's Hospital, 213000 Changzhou, Jiangsu, China.
authors: Rihua
authors: R
authors: Zhang
authors: Dongming
authors: D
authors: Su
authors: Weidong
authors: W
authors: Zhu
authors: Qiong
authors: Q
authors: Huang
authors: Menglan
authors: M
authors: Liu
authors: Yi
authors: Y
authors: Xue
authors: Yuanyuan
authors: Y
authors: Zhang
authors: Dong
authors: D
authors: li
authors: Allan
authors: A
authors: Zhao
authors: Yun
authors: Y
authors: Liu
mesh_terms: D050153:Abdominal Fat; D050156:Adipogenesis / Q000187:drug effects*; D000818:Animals; D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000096:biosynthesis; D002478:Cells, Cultured; D059305:Diet, High-Fat; D004967:Estrogens / Q000494:pharmacology*; D050556:Fatty Acid-Binding Proteins / Q000096:biosynthesis; D005260:Female; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D024821:Metabolic Syndrome; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010052:Ovariectomy; D047495:PPAR gamma / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D009418:S100 Proteins / Q000096:biosynthesis* / Q000235:genetics; D014158:Transcription, Genetic / Q000187:drug effects; D015430:Weight Gain / Q000187:drug effects
chemical_list: D022763:CCAAT-Enhancer-Binding Protein-alpha; D004967:Estrogens; C524662:FABP4 protein, rat; C493411:Fabp4 protein, mouse; D050556:Fatty Acid-Binding Proteins; D047495:PPAR gamma; D009418:S100 Proteins; C570791:S100A16 protein, rat; D005947:Glucose
keywords: S100A16; estrogen; metabolic syndrome