Departamento de Farmacologia. Facultad de Medicina, Universidad Autonoma de Madrid, Arzobispo Morcillo 4, 28029 Madrid, Spain.
Curr Vasc Pharmacol. 2014 May;12(3):427-37. doi: 10.2174/1570161112666140423221319.
Microvascular abnormalities, both in function and structure, lead to impaired tissue perfusion that may affect multiple tissues and organs and seem to be involved in target-organ damage and complications observed in obesity and insulin resistance. In general, vascular remodeling of small arteries associated to cardiometabolic diseases seems to be hypertrophic and it is associated to increased extracellular matrix deposition, although specific vascular beds might show different structural patterns. The mechanisms by which obesity, insulin resistance and/or hyperinsulimemia determine vascular disease are not clear yet but might include hemodynamic factors such as hypertension, activation of the sympathetic nervous and the renin-angiotensin-aldosterone systems, metabolic factors such as insulin and advanced glycation end products and other factors such as adipokines, inflammation or oxidative stress. Exercise and weight loss as well as blockade of the renin-angiotensin system seem to be efficient actions to correct vascular alterations in patients. This review aims to examine the existing literature on structural alterations in small vessels associated to insulin resistance and obesity. A description about the underlying mechanisms possibly responsible of the vascular alterations is also provided. Moreover, effects of pharmacological and non pharmacological strategies that could modify these vascular alterations are summarized.
微血管功能和结构的异常导致组织灌注受损，可能影响多个组织和器官，并且似乎与肥胖和胰岛素抵抗所观察到的靶器官损伤和并发症有关。一般来说，与代谢性心血管疾病相关的小动脉血管重构似乎是肥厚性的，并且与细胞外基质沉积增加有关，尽管特定的血管床可能表现出不同的结构模式。肥胖、胰岛素抵抗和/或高胰岛素血症确定血管疾病的机制尚不清楚，但可能包括血流动力学因素，如高血压、交感神经系统和肾素-血管紧张素-醛固酮系统的激活、代谢因素，如胰岛素和晚期糖基化终产物以及其他因素，如脂肪因子、炎症或氧化应激。运动和减肥以及阻断肾素-血管紧张素系统似乎是纠正患者血管异常的有效方法。本综述旨在检查与胰岛素抵抗和肥胖相关的小血管结构改变的现有文献。还提供了对可能导致血管改变的潜在机制的描述。此外，总结了可改变这些血管改变的药理学和非药理学策略的效果。
