活性氧在代谢综合征脂肪细胞功能障碍发病机制中的作用。药物矫正的前景[j]。

E S Prokudina, L N Maslov, V V Ivanov, I D Bespalova, D S Pismennyi, N S Voronkov
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引用次数: 11

摘要

氧化应激诱导脂肪细胞胰岛素抵抗,增加脂肪细胞分泌瘦素、IL-6、TNF-α。在活性氧的作用下,脂肪细胞分泌的脂联素减少。代谢综合征导致脂肪组织氧化应激,一方面是由于脂肪细胞nadph氧化酶激活活性氧的产生,另一方面是由于脂肪细胞的抗氧化防御能力降低。研究发现,肥胖本身可以诱发氧化应激。慢性应激、糖皮质激素、矿物皮质激素、血管紧张素- ii、TNF-α在脂肪细胞氧化应激的发病机制中起重要作用。二甲双胍仍然是治疗胰岛素抵抗的良方。氯沙坦治疗代谢综合征的阳性结果。抗氧化剂和类黄酮对实验性代谢综合征的病程有积极影响。
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[The Role of Reactive Oxygen Species in the Pathogenesis of Adipocyte Dysfunction in Metabolic Syndrome. Prospects of Pharmacological Correction].

It is established that oxidative stress induces insulin resistance of adipocytes, increases secretion leptin, IL-6, TNF-α by adipocytes. Adiponectin secretion by adipocytes is reduced after the action of reactive oxygen species. Metabolic syndrome contributes to oxidative stress in adipose tissue, on the one hand due to the activation of production of reactive oxygen species by adipocyte NADPH-oxidase, and on the other hand by reducing the antioxidant defense adipocytes. It is found that obesity itself can induce oxidative stress. Chronic stress, glucocorticoids, mineralocorticoids, angiotensin-II, TNF-α play an important role in the pathogenesis of oxidative stress of adipocytes. Metformin remains the cure for the treatment of insulin resistance. The positive results in the treatment of metabolic syndrome by losartan were obtained. Antioxidants and flavonoids exhibit a positive impact on the course of the experimental metabolic syndrome.

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