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脂肪因子和游离脂肪酸通过增加人类成熟脂肪细胞中微小RNA-21的表达来调节胰岛素敏感性。

Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes.

作者信息

Zhang Nannan, Zhang Naijian, Song Leilei, Xie Hui, Zhao Chao, Li Sujuan, Zhao Wenxi, Zhao Yaping, Gao Chunlin, Xu Guangfeng

机构信息

Department of Laboratory Medicine, The 82nd Hospital of The People's Liberation Army, Huaian, Jiangsu 223001, P.R. China.

Department of Pediatrics, Jinling Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210002, P.R. China.

出版信息

Mol Med Rep. 2017 Aug;16(2):2254-2258. doi: 10.3892/mmr.2017.6769. Epub 2017 Jun 14.

DOI:10.3892/mmr.2017.6769
PMID:28627656
Abstract

Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy‑source materials contribute to obesity and obesity‑associated insulin resistance. MicroRNAs (miRs) are endogenous 20‑ to 25‑nucleotide non‑coding RNAs associated with fat metabolism. It has been indicated that miR‑21 is associated with adipogenesis and metabolic syndrome. In the present study, the expression of miR‑21 in human mature adipocytes was analyzed using reverse transcription quantitative‑polymerase chain reaction following treatment with adipokines, including tumor necrosis factor (TNF)‑α, interleukin (IL)‑6, leptin, resistin and energy source materials, including free fatty acids (FFAs) and glucose. The current study demonstrated that the expression of miR‑21 in human mature adipocytes was upregulated following treatment with TNF‑α, IL‑6, leptin, resistin and FFAs. However, low‑ and high‑glucose did not have an effect on miR‑21 expression. These results confirmed that TNF‑α, IL‑6, leptin, resistin and FFAs may contribute to obesity and obesity‑associated insulin resistance via upregulating miR‑21 in human mature adipocytes. Therefore, miR‑21 may be a key regulatory factor of obesity and obesity‑associated insulin resistance, and represents a potential therapeutic target for the treatment of these disorders.

摘要

肥胖是一个全球性的公共卫生问题,可能导致多种并发症。先前的研究表明,脂肪因子和能量来源物质与肥胖及肥胖相关的胰岛素抵抗有关。微小RNA(miR)是与脂肪代谢相关的内源性20至25个核苷酸的非编码RNA。已有研究表明,miR-21与脂肪生成和代谢综合征有关。在本研究中,在用包括肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6、瘦素、抵抗素等脂肪因子以及包括游离脂肪酸(FFA)和葡萄糖等能量来源物质处理后,使用逆转录定量聚合酶链反应分析了人成熟脂肪细胞中miR-21的表达。当前研究表明,在用TNF-α、IL-6、瘦素、抵抗素和FFA处理后人成熟脂肪细胞中miR-21的表达上调。然而,低糖和高糖对miR-21的表达没有影响。这些结果证实,TNF-α、IL-6、瘦素、抵抗素和FFA可能通过上调人成熟脂肪细胞中的miR-21而导致肥胖及肥胖相关的胰岛素抵抗。因此,miR-21可能是肥胖及肥胖相关胰岛素抵抗的关键调节因子,并且代表了治疗这些疾病的潜在治疗靶点。

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