The microcirculation in adipose tissue inflammation.
The microcirculation in adipose tissue inflammation.
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DOI：
10.1007/s11154-013-9236-x
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发表时间：
2013-03
影响因子：
8.2
通讯作者：
Scalia R
中科院分区：
文献类型：
--
作者：
Scalia R
在大多数人类中，肥胖与包括脂肪组织在内的几个器官组织中发生的慢性低度炎症反应有关。骨髓来源的白细胞(粒细胞、单核细胞、淋巴细胞)渗入扩张的脂肪库似乎是肥胖症炎症的一个组成部分。循环中的白细胞主要通过微循环中的毛细血管后小静脉侵入器官组织。毛细血管后小静脉的内皮细胞通过在其管腔表面置换结合循环白细胞上表达的黏附受体的黏附分子来起到阻止白细胞黏附和外渗的作用。一些研究肥胖对微循环的影响的研究已经证明，在肥胖的实验动物模型中，以及在肥胖的人类中，都会发生微血管功能障碍。然而，到目前为止，正在进行的假设和研究设计都支持这样的观点，即微血管改变是脂肪组织功能障碍的次要因素。事实上，科学文献中有大量数据支持微血管功能障碍可能先于肥胖并导致脂肪组织炎症的概念。通过对已发表的关键数据的回顾，本文前瞻性地提出了这样一个概念，即在体重增加和明显肥胖之前，微循环的血管内皮细胞敏锐地激活炎症途径，启动白细胞在内脏脂肪组织中的渗透。对不同微循环的解剖和生理异质性也进行了讨论，以了解肥胖如何导致内脏和皮下脂肪库中不同的炎症表型。
In most humans, obesity is associated with a chronic low-grade inflammatory reaction occurring in several organ tissues, including the adipose tissue. Infiltration of bone marrow derived leukocytes (granulocytes, monocytes, lymphocytes) into expanding adipose depots appears to be an integral component of inflammation in obesity. Circulating leukocytes invade organ tissues mainly through post-capillary venules in the microcirculation. The endothelium of the post-capillary venules acts as a gatekeeper to leukocyte adhesion and extravasation by displacing on its luminal surface adhesion molecules that bind the adhesive receptors expressed on circulating leukocytes. Several studies investigating the impact of obesity on the microcirculation have demonstrated the occurrence of microvascular dysfunction in experimental animal model of obesity, as well as in obese humans. To date though, working hypotheses and study designs have favored the view that microvascular alterations are secondary to adipose tissue dysfunction. Indeed, a significant amount of data exists in the scientific literature to support the concept that microvascular dysfunction may precede and cause adipose tissue inflammation in obesity. Through review of key published data, this article prospectively presents the concept that in response to nutrients overload the vascular endothelium of the microcirculation acutely activates inflammatory pathways that initiate infiltration of leukocytes in visceral adipose tissue, well before weight gain and overt obesity. The anatomical and physiological heterogeneity of different microcirculations is also discussed toward the understanding of how obesity induces different inflammatory phenotypes in visceral and subcutaneous fat depots.
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