Is oxidative stress of adipocytes a cause or a consequence of the metabolic syndrome?

Is oxidative stress of adipocytes a cause or a consequence of the metabolic syndrome?
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DOI:
10.1016/j.jcte.2018.11.001
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发表时间:
2019-03
影响因子:
3
通讯作者:
Oeltgen PR
Oeltgen PR
中科院分区:
其他
文献类型:
--
作者:
Maslov LN;Naryzhnaya NV;Boshchenko AA;Popov SV;Ivanov VV;Oeltgen PR

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代谢综合征伴随着动物和人类的氧化应激。实验性代谢综合征中ROS的主要来源是NADPH氧化酶和可能的脂肪细胞线粒体。现已证实氧化应激诱导脂肪细胞的胰岛素抵抗并增加脂肪细胞分泌瘦素、MCP-1、IL-6和TNF-α。已经确定氧化应激诱导脂肪细胞产生脂联素的减少。也有研究表明,肥胖本身可以诱导氧化应激。氧化应激可引起脂肪细胞内信号转导的改变,从而导致脂肪细胞胰岛素抵抗的形成。慢性应激、糖皮质激素、盐皮质激素、血管紧张素-II、TNF-α等也在脂肪细胞氧化应激的发病机制中发挥重要作用。氧化应激不仅是代谢综合征的后果,也是代谢综合征发病的原因和基础环节。
Metabolic syndrome is accompanied by oxidative stress in animals and humans. The main source of ROS in experimental metabolic syndrome is NADPH oxidase and possibly adipocyte mitochondria. It is now documented that oxidative stress induces insulin resistance of adipocytes and increases secretion of leptin, MCP-1, IL-6, and TNF-α by adipocytes. It was established that oxidative stress induces a decrease in adiponectin production by adipocytes. It has also been shown that obesity itself can induce oxidative stress. Oxidative stress can cause an alteration of intracellular signaling in adipocytes that apparently leads to the formation of insulin resistance of adipocytes. Chronic stress, glucocorticoids, mineralocorticoids, angiotensin-II, TNF-α also play an important role in the pathogenesis of oxidative stress of adipocytes. Oxidative stress is not only a consequence of metabolic syndrome, but also a reason and a foundational link in the pathogenesis of the metabolic syndrome.
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