Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Department of Pharmaceutical and Pharmacological Sciences, University of Padova, Padova, Italy.
J Clin Endocrinol Metab. 2019 Feb 1;104(2):341-348. doi: 10.1210/jc.2018-00512.
Endothelium guarantees vascular homeostasis by the opposite action of substances by vasodilating/antithrombogenic and vasoconstricting/prothrombotic activities. Obesity is characterized by endothelial dysfunction associated with a condition of vascular low-grade inflammation.
Analysis of available basic or clinical papers published in peer-reviewed international journals on microcirculation and obesity.
Vascular low-grade inflammation, which characterizes obesity, is secondary to abnormal production of proinflammatory cytokines, including TNF-α. TNF-α, generated either in small vessels or within the perivascular adipose tissue (PVAT) of patients with obesity, stimulates reactive oxygen species generation, mainly through NAD(P)H oxidase activation, which in turn reduces nitric oxide (NO) availability. These aspects are highlighted by the insulin resistance status and macronutrient intake that characterize the obesity condition. Oxidant excess has also been proposed as a mechanism whereby TNF-α interferes with the endothelin-1/NO system at the level of small vessels from patients with obesity.
In obesity, microvasculature from visceral fat is an important source of low-grade inflammation and oxidative stress that, together with the PVAT, directly contribute to vascular changes, favoring the development and acceleration of the vascular atherothrombotic process in this clinical condition.
内皮通过舒张/抗血栓和收缩/促血栓活性的相反作用来保证血管的稳态。肥胖的特征是内皮功能障碍，伴有血管低度炎症状态。
对发表在同行评议的国际微循环和肥胖杂志上的可用基础或临床论文进行分析。
肥胖患者的血管低度炎症继发于促炎细胞因子（包括 TNF-α）的异常产生。肥胖患者的小血管或血管周围脂肪组织（PVAT）中产生的 TNF-α刺激活性氧的产生，主要通过 NAD（P）H 氧化酶的激活，而这反过来又降低了一氧化氮（NO）的可用性。这些方面突出了肥胖状况的胰岛素抵抗状态和宏量营养素摄入的特点。氧化应激过剩也被提出是 TNF-α在肥胖患者的小血管水平干扰内皮素 1/NO 系统的机制之一。
在肥胖中，内脏脂肪的微血管是低度炎症和氧化应激的重要来源，与 PVAT 一起，直接导致血管变化，有利于这种临床状况下血管动脉粥样硬化血栓形成过程的发展和加速。
