Expression of microRNA-26b, an obesity-related microRNA, is regulated by free fatty acids, glucose, dexamethasone and growth hormone in human adipocytes

Xu,Guangfeng; Shi,Chunmei; Ji,Chenbo; Song,Guixian; Chen,Ling; Yang,Lei; Zhao,Yaping; Guo,Xirong

doi:10.3892/mmr.2014.2204

Expression of microRNA-26b, an obesity-related microRNA, is regulated by free fatty acids, glucose, dexamethasone and growth hormone in human adipocytes

Authors:
- Guangfeng Xu
- Chunmei Shi
- Chenbo Ji
- Guixian Song
- Ling Chen
- Lei Yang
- Yaping Zhao
- Xirong Guo
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Affiliations: Department of Laboratory Medicine, The 82nd Hospital of The People's Liberation Army, Huaian, Jiangsu 223001, P.R. China, Department of Children Health Care, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Institute of Pediatrics, Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China
Published online on: May 2, 2014 https://doi.org/10.3892/mmr.2014.2204
Pages: 223-228

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Abstract

MicroRNAs (miRNAs) are short non-coding RNAs that are involved in numerous biological processes, including obesity and insulin resistance. miR-26b is an obesity-related intronic miRNA located in the intron of the carboxy‑terminal domain, RNA polymerase II, polypeptide A, small phosphatase 1 gene. miR-26b is abundantly expressed in mice and mature human adipocytes, and is associated with the expression of adipokines. In the present study, the effects of energy-source materials and hormones associated with obesity, on miR-26b expression were investigated. It was demonstrated that free fatty acids (FFAs), glucose, glucocorticoids and growth hormone (GH) downregulate the expression of miR-26b in human adipocytes. The results indicate that the expression of miR-26b is affected by a variety of factors that are correlated with obesity and insulin sensitivity. Therefore, miR-26b may be an important mediator in the development of obesity‑associated insulin resistance.

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