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
-
Figure 1
Images of visceral fat cells and liver cells. (A) Images of visceral fat cells after hematoxylin and eosin (HE) staining. The body weights of all rats were monitored every week and visceral fat weight was measured when the mice were anesthetized with Nembutal (100 mg/kg). The images are shown at 400× magnification. (B) Histological images of the livers of rats fed chow and HFD, as visualized by HE staining. All the images are shown at 400× magnification.
-
Figure 2
The effect of E2 on systemic glucose homeostasis. (A) Glucose level of rats under the chow conditions. (B) Insulin level of rats under the chow conditions. (C) Glucose level of rats under the HFD conditions. (D) Insulin level of rats under the HFD conditions. Results are expressed as the mean±s.d. *P<0.05 compared with the corresponding control group.
-
Figure 3
The effect of E2 on the expression of adipogenesis marker genes of PPARγ, C/EBPα, and aP2 in fat tissue. The protein expression of S100A16 (A), PPARγ (B), C/EBPα (E), and aP2 (G) was analyzed with western blotting. (C, D, F and H) Relative expression of S100A16, PPARγ, C/EBPα, and aP2 based on grayscale analysis. α-Tubulin was used as the control. Lanes 1 and 2, normal control rats on the chow diet; lanes 3 and 4, normal control rats on the HFD; lanes 5 and 6, OVX rats on the chow diet; lanes 7 and 8, OVX rats on the HFD; lanes 9 and 10, OVX rats treated with E2 on the chow diet; lanes 11 and 12, OVX rats treated with E2 on the HFD. Results are expressed as the mean±s.d. *P<0.05 compared with the corresponding control group.
-
Figure 4
E2-induced suppression of adipogenesis via S100A16 inhibition. (A) Western blot assays of S100A16 expression in the protein extracts collected from S100A16Tg+/+ MEFs treated with different concentrations of E2 (0, 50, 100, 200, 400, and 800 pg/ml) for 24 h. (B) Western blot assays of S100A16 expression in the protein extracts collected from S100A16Tg+/+ MEFs treated with 100 pg/ml E2 for different times (0, 12, 24, 48, and 72 h). α-Tubulin was used as the control. (E) Western blot assays of S100A16 expression in the protein extracts collected from C57BL/6 MEFs treated with different concentrations of E2 (0, 50, 100, 200, and 400 pg/ml) for 24 h. (C, D and F) Relative expression of S100A16 based on grayscale analysis. (G and H) mRNA levels of S100A16 S100A16Tg+/+ MEFs and normal MEFs, respectively, treated with E2. (I) Oil Red O staining patterns for MEFs from C57BL/6 and S100A16Tg+/+ mice treated with different concentrations of E2 and induced to differentiate into adipocytes. Photographs were taken under a light microscope with 200× magnification. (J) Triglyceride accumulation in the MEFs was significantly higher in the S100A16Tg+/+ MEFs for all E2 concentrations. *P<0.05 compared with the corresponding control group.
-
Figure 5
Inhibition of S100A16 transcription by E2. (A) The 1500-bp promoter region of S100A16 shows four estrogen receptor (ER) binding sites. (B) Results of the S100A16 luciferase reporter assay; S100A16 expression was reduced in the presence of E2, and this effect was ameliorated by the addition of tamoxifen. Results are expressed as mean±s.d. *indicates statistical significance (P<0.05 ).
- © 2014 The authors
