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DJ-1参与脂肪生成和肥胖诱导的炎症反应。

DJ-1 contributes to adipogenesis and obesity-induced inflammation.

作者信息

Kim Jung-Min, Jang Hyun-Jun, Choi Soo Youn, Park Soo-Ah, Kim Il Shin, Yang Yong Ryoul, Lee Yong Hwa, Ryu Sung Ho, Suh Pann-Ghill

机构信息

1] School of Nano-Bioscience & Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea [2].

1] School of Nano-Bioscience & Chemical Engineering, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea [2] Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.

出版信息

Sci Rep. 2014 Jun 13;4:4805. doi: 10.1038/srep04805.

DOI:10.1038/srep04805
PMID:24925581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4055892/
Abstract

Adipose tissue functions as an endocrine organ, and the development of systemic inflammation in adipose tissue is closely associated with metabolic diseases, such as obesity and insulin resistance. Accordingly, the fine regulation of the inflammatory response caused by obesity has therapeutic potential for the treatment of metabolic syndrome. In this study, we analyzed the role of DJ-1 (PARK7) in adipogenesis and inflammation related to obesity in vitro and in vivo. Many intracellular functions of DJ-1, including oxidative stress regulation, are known. However, the possibility of DJ-1 involvement in metabolic disease is largely unknown. Our results suggest that DJ-1 deficiency results in reduced adipogenesis and the down-regulation of pro-inflammatory cytokines in vitro. Furthermore, DJ-1-deficient mice show a low-level inflammatory response in the high-fat diet-induced obesity model. These results indicate previously unknown functions of DJ-1 in metabolism and therefore suggest that precise regulation of DJ-1 in adipose tissue might have a therapeutic advantage for metabolic disease treatment.

摘要

脂肪组织作为一个内分泌器官发挥作用,脂肪组织中全身炎症的发展与肥胖和胰岛素抵抗等代谢性疾病密切相关。因此,对肥胖引起的炎症反应进行精细调节具有治疗代谢综合征的潜力。在本研究中,我们在体外和体内分析了DJ-1(PARK7)在与肥胖相关的脂肪生成和炎症中的作用。DJ-1的许多细胞内功能,包括氧化应激调节,是已知的。然而,DJ-1参与代谢性疾病的可能性在很大程度上尚不清楚。我们的结果表明,DJ-1缺乏导致体外脂肪生成减少和促炎细胞因子下调。此外,在高脂饮食诱导的肥胖模型中,DJ-1缺陷小鼠表现出低水平的炎症反应。这些结果表明DJ-1在代谢中具有以前未知的功能,因此表明在脂肪组织中精确调节DJ-1可能对代谢性疾病治疗具有治疗优势。

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