Mertens Ilse, Van Gaal Luc F
Department of Diabetology, Metabolism and Clinical Nutrition, Faculty of Medicine, Antwerp University Hospital, University of Antwerp, Antwerp, Belgium.
Semin Vasc Med. 2005 Feb;5(1):48-55. doi: 10.1055/s-2005-871741.
An increased amount of deep abdominal visceral fat has generally been accepted as an important cardiovascular risk factor, and disturbances in hemostasis and fibrinolysis have been suggested to play a role. Fibrinogen and von Willebrand factor, representatives of the hemostatic system, and plasminogen activator inhibitor 1 (PAI-1), as the most important inhibitor of the fibrinolytic system, have been associated with visceral obesity, with the most convincing evidence found for the involvement of PAI-1. The association with fibrinogen and von Willebrand factor has been suggested to be merely a reflection of the association with inflammation and endothelial dysfunction. The fact that PAI-1 is secreted by adipose tissue has attracted much attention. The increase of PAI-1 in visceral obesity could be because visceral adipose tissue produces more PAI-1 compared with subcutaneous abdominal adipose tissue. The contribution of other cell types such as hepatocytes or endothelial cells is probably more important, with stimulation of PAI-1 production by different components of the metabolic syndrome. PAI-1 secretion by adipose tissue has been suggested to have a more local effect, playing a role in tissue remodeling during the development of obesity.
腹部深层内脏脂肪量增加通常被认为是一个重要的心血管危险因素，并且有人提出止血和纤维蛋白溶解功能紊乱也起一定作用。作为止血系统代表的纤维蛋白原和血管性血友病因子，以及作为纤维蛋白溶解系统最重要抑制剂的纤溶酶原激活物抑制剂1（PAI-1），都与内脏肥胖有关，其中关于PAI-1参与的证据最具说服力。有人认为与纤维蛋白原和血管性血友病因子的关联仅仅是与炎症和内皮功能障碍关联的一种反映。PAI-1由脂肪组织分泌这一事实引起了广泛关注。内脏肥胖中PAI-1增加可能是因为与腹部皮下脂肪组织相比，内脏脂肪组织产生更多的PAI-1。其他细胞类型（如肝细胞或内皮细胞）的作用可能更重要，代谢综合征的不同成分会刺激PAI-1的产生。脂肪组织分泌PAI-1被认为具有更局部的作用，在肥胖发生过程中的组织重塑中发挥作用。
