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2型糖尿病中与肥胖相关的低度炎症:原因与后果

Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences.

作者信息

van Greevenbroek M M J, Schalkwijk C G, Stehouwer C D A

机构信息

Department of Internal Medicine & Laboratory for Metabolism and Vascular Medicine, Maastricht University Medical Centre, Maastricht, the Netherlands.

出版信息

Neth J Med. 2013 May;71(4):174-87.

PMID:23723111
Abstract

The epidemic of overweight and obesity is a major problem because of the plethora of health and economic issues that it induces. Key among these is the sharply increasing prevalence of type 2 diabetes (T2D) and cardiovascular disease. The development of T2D is characterised by two processes: 1) insulin resistance, resulting from impaired insulin signalling and leading to an increased demand for insulin, which must be met by increased insulin production by pancreatic β-cells (compensatory β-cell function); and 2) β-cell dysfunction, with T2D developing when the amount of insulin that is produced is insufficient to meet the demand. Overweight and obesity, especially in case of abdominal fat accumulation, are associated with systemic low-grade inf lammation. This low-grade inf lammation is characterised by, among other things, higher levels of circulating proinflammatory cytokines and fatty acids. These can interfere with normal insulin function and thereby induce insulin resistance, and have also been implicated in β-cell dysfunction. This review focuses on the known and emerging relations between inflammation and T2D. We first discuss current views on the effects of fat distribution on adipose tissue inflammation and adipose tissue dysfunction. Next we focus on the detrimental roles of proinflammatory cytokines and fatty acids on insulin signalling and β-cell function. In the last part of this review we provide some insight into novel players in (the initiation of) inflammation in overweight and obesity, and their effects on T2D and vascular dysfunction.

摘要

超重和肥胖的流行是一个重大问题,因为它引发了大量的健康和经济问题。其中关键的是2型糖尿病(T2D)和心血管疾病的患病率急剧上升。T2D的发展具有两个特征:1)胰岛素抵抗,由胰岛素信号受损导致,进而导致对胰岛素的需求增加,这必须通过胰腺β细胞增加胰岛素分泌来满足(代偿性β细胞功能);2)β细胞功能障碍,当产生的胰岛素量不足以满足需求时,T2D就会发展。超重和肥胖,尤其是腹部脂肪堆积的情况下,与全身低度炎症有关。这种低度炎症的特征包括,除其他外,循环中促炎细胞因子和脂肪酸水平升高。这些物质会干扰正常的胰岛素功能,从而诱发胰岛素抵抗,并且也与β细胞功能障碍有关。本综述重点关注炎症与T2D之间已知的和新出现的关系。我们首先讨论目前关于脂肪分布对脂肪组织炎症和脂肪组织功能障碍影响的观点。接下来,我们关注促炎细胞因子和脂肪酸对胰岛素信号传导和β细胞功能的有害作用。在本综述的最后部分,我们深入探讨了超重和肥胖炎症(起始阶段)中的新参与者,以及它们对T2D和血管功能障碍的影响。

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