Department of Medicine, The University of Hong Kong, 21 Sassoon Road, Pokfulam, Hong Kong SAR.
Rev Endocr Metab Disord. 2013 Mar;14(1):49-58. doi: 10.1007/s11154-012-9230-8.
There is a close anatomical and functional relationship between adipose tissue and blood vessels. The crosstalk between these two organs is vital to both metabolic and vascular homeostasis. On the one hand, adipose tissue is highly vascularized, and maintenance of ample supply of blood flow is essential for both expansion and metabolic functions of adipose tissue. Vascular endothelium also secretes many factors to regulate adipogenesis and adipose tissue remodeling. On the other hand, almost all blood vessels are surrounded by perivascular adipose tissue (PVAT), which regulates vascular function by producing a large number of "vasocrine" molecules. Under the normal conditions, PVAT exerts its anti-contractile effects by release of vasorelaxants (such as adipocyte-derived relaxation factors and adiponectin) that promote both endothelium-dependent and -independent relaxations of blood vessels. However, PVAT in obesity becomes highly inflamed and induces vascular dysfunction by augmented secretion of vasoconstriction factors (such as the major components of renin-angiotensinogen-aldosterone system and superoxide) and pro-inflammatory adipokines (such as TNF-α and adipocyte fatty acid binding protein), the latter of which are important contributors to endothelial activation, vascular inflammation and neointimal formation. Furthermore, several adipocyte-derived adipokines impair vascular function indirectly, by acting in the brain to activate sympathetic nerve system (such as leptin) or by exerting their actions in major metabolic organs to induce vascular insulin resistance, which in turn aggravates endothelial dysfunction. Aberrant secretion of adipokines and other vasoactive factors in adipose tissue is a major contributor to the onset and progression of obesity-related metabolic and vascular complications.
脂肪组织和血管之间存在密切的解剖和功能关系。这两个器官之间的相互作用对于代谢和血管稳态都至关重要。一方面，脂肪组织高度血管化，充足的血流供应对于脂肪组织的扩张和代谢功能都是必不可少的。血管内皮细胞也分泌许多因子来调节脂肪生成和脂肪组织重塑。另一方面，几乎所有的血管都被血管周围脂肪组织（PVAT）包围，后者通过产生大量的“血管内分泌”分子来调节血管功能。在正常情况下，PVAT 通过释放血管舒张因子（如脂肪细胞衍生的舒张因子和脂联素）来发挥其抗收缩作用，促进血管内皮依赖性和非依赖性舒张。然而，肥胖症中的 PVAT 会发生高度炎症，并通过增强血管收缩因子（如肾素-血管紧张素原-醛固酮系统和超氧化物的主要成分）和促炎脂肪因子（如 TNF-α和脂肪细胞脂肪酸结合蛋白）的分泌而导致血管功能障碍，后者是内皮细胞激活、血管炎症和新生内膜形成的重要因素。此外，几种脂肪细胞衍生的脂肪因子通过在大脑中作用激活交感神经系统（如瘦素）或在主要代谢器官中发挥作用诱导血管胰岛素抵抗，从而间接损害血管功能，这反过来又加重了内皮功能障碍。脂肪组织中脂肪因子和其他血管活性因子的异常分泌是肥胖相关代谢和血管并发症发生和进展的主要原因。
