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脂肪细胞更新中的潜伏性炎症和缺陷作为肥胖相关胰岛素抵抗的一种机制。

Latent Inflammation and Defect in Adipocyte Renewal as a Mechanism of Obesity-Associated Insulin Resistance.

机构信息

Institute of Experimental Cardiology, National Medical Research Center of Cardiology, Ministry of Healthcare of the Russian Federation, Moscow, 121552, Russia.

Diabetes Institute, National Medical Research Center of Endocrinology, Moscow, 117036, Russia.

出版信息

Biochemistry (Mosc). 2019 Nov;84(11):1329-1345. doi: 10.1134/S0006297919110099.

Abstract

Obesity is a major risk factor for type 2 diabetes and metabolic syndrome and an essential medical and social problem. In the first part of the review, we briefly highlight the biochemical basis of metabolic disbalance in obesity and evolution of our views on the mechanisms of insulin resistance development in insulin-sensitive tissues. Because obesity relates to the disturbance in the normal physiology of fat tissue, the second part of the review focuses on latent inflammation that develops in obesity and is supported by immune cells. Finally, the problem of adipocyte hypertrophy, reduced regenerative potential of fat progenitor cells, and impaired renewal of fat depots is discussed in the context of type 2 diabetes pathogenesis.

摘要

肥胖是 2 型糖尿病和代谢综合征的主要危险因素,也是一个重要的医学和社会问题。在综述的第一部分,我们简要地强调了肥胖症中代谢失衡的生化基础,以及我们对胰岛素敏感组织中胰岛素抵抗发展机制的看法的演变。由于肥胖与脂肪组织正常生理学的紊乱有关,因此综述的第二部分侧重于肥胖症中发生的潜在炎症,这些炎症得到免疫细胞的支持。最后,在 2 型糖尿病发病机制的背景下,讨论了脂肪细胞肥大、脂肪祖细胞再生潜力降低以及脂肪储存更新受损的问题。

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