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Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines

  • Authors:
    • Nan Gu
    • Lianghui You
    • Chunmei Shi
    • Lei Yang
    • Lingxia Pang
    • Xianwei Cui
    • Chenbo Ji
    • Wen Zheng
    • Xirong Guo
  • View Affiliations / Copyright

    Affiliations: Nanjing Maternity and Child Health Care Institute, Nanjing Maternity and Child Health Care Hospital Affiliated With Nanjing Medical University, Nanjing, Jiangsu 210004, P.R. China, Maternity and Child Health Hospital of Yancheng, Yancheng, Jiangsu 224002, P.R. China
    Copyright: © Gu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1180-1186
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    Published online on: June 8, 2016
       https://doi.org/10.3892/mmr.2016.5379
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Abstract

Obesity is associated with a notable risk for disease, including risk of cardiovascular disorders, type 2 diabetes mellitus (T2DM) and hypertension. Adipose tissue modulates the metabolism by releasing free fatty acids (FFAs) and adipokines, including leptin, resistin, tumor necrosis factor-α (TNF-α) and interleukin 6 (IL‑6). Altered secretion patterns of FFAs and adipokines have been demonstrated to result in obesity‑associated insulin resistance (IR) and inflammatory responses. MicroRNA-199a-3p (miR)-199a-3p expression is significantly induced in differentiated human adipose-derived mesenchymal stem cells and indicates the association with T2DM. However, the association between miR-199a-3p levels in adipocytes and obesity‑associated IR, as well as inflammatory responses remains to be elucidated. The present study observed an elevation of miR‑199a‑3p expression level in mature human adipocytes (visceral) compared with pre-adipocytes. In addition, miR‑199a‑3p expression was higher in visceral adipose deposits from obese subjects. FFA, TNF-α, IL‑6 and leptin significantly induced miR‑199a‑3p expression in mature human adipocytes, while resistin had the opposite effect. miR‑199a‑3p may represent a factor in the modulation of obesity‑associated IR and inflammatory responses.
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Copy and paste a formatted citation
Spandidos Publications style
Gu N, You L, Shi C, Yang L, Pang L, Cui X, Ji C, Zheng W and Guo X: Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines. Mol Med Rep 14: 1180-1186, 2016.
APA
Gu, N., You, L., Shi, C., Yang, L., Pang, L., Cui, X. ... Guo, X. (2016). Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines. Molecular Medicine Reports, 14, 1180-1186. https://doi.org/10.3892/mmr.2016.5379
MLA
Gu, N., You, L., Shi, C., Yang, L., Pang, L., Cui, X., Ji, C., Zheng, W., Guo, X."Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines". Molecular Medicine Reports 14.2 (2016): 1180-1186.
Chicago
Gu, N., You, L., Shi, C., Yang, L., Pang, L., Cui, X., Ji, C., Zheng, W., Guo, X."Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines". Molecular Medicine Reports 14, no. 2 (2016): 1180-1186. https://doi.org/10.3892/mmr.2016.5379
Copy and paste a formatted citation
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Spandidos Publications style
Gu N, You L, Shi C, Yang L, Pang L, Cui X, Ji C, Zheng W and Guo X: Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines. Mol Med Rep 14: 1180-1186, 2016.
APA
Gu, N., You, L., Shi, C., Yang, L., Pang, L., Cui, X. ... Guo, X. (2016). Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines. Molecular Medicine Reports, 14, 1180-1186. https://doi.org/10.3892/mmr.2016.5379
MLA
Gu, N., You, L., Shi, C., Yang, L., Pang, L., Cui, X., Ji, C., Zheng, W., Guo, X."Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines". Molecular Medicine Reports 14.2 (2016): 1180-1186.
Chicago
Gu, N., You, L., Shi, C., Yang, L., Pang, L., Cui, X., Ji, C., Zheng, W., Guo, X."Expression of miR-199a-3p in human adipocytes is regulated by free fatty acids and adipokines". Molecular Medicine Reports 14, no. 2 (2016): 1180-1186. https://doi.org/10.3892/mmr.2016.5379
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