Laboratory of Physiology, Faculty of Medicine, Institute of Biomedical Imaging and Life Sciences (IBILI), University of Coimbra , Portugal.
Arch Physiol Biochem. 2014 Feb;120(1):1-11. doi: 10.3109/13813455.2013.838971. Epub 2013 Sep 25.
In the last years, several studies unravelled many aspects of adipose tissue pathophysiology in metabolic diseases. Some studies suggested hypoxia as one of such aspects, despite the exact mechanisms and pathophysiological significance is still partially unknown. Adipose tissue was shown to be hypoxic in obesity, mainly resulting from adipocyte hypertrophy, leading to increased activation of inflammatory pathways. In animal and cell models, hypoxia-induced inflammation was shown to lead to endocrine alterations and dysmetabolism. However, recent evidences suggest that instead of a simple low oxygenation theory, adipose tissue microvasculature may be regulated by a series of factors, including vasoactive factors like angiotensin II, angiogenesis and glycation, among others. This review summarizes the current knowledge about the role of these factors in the regulation of adipose tissue irrigation and the functional consequences of adipose tissue microvascular dysfunction.
在过去的几年中，多项研究揭示了代谢性疾病中脂肪组织病理生理学的许多方面。一些研究表明缺氧是其中一个方面，尽管确切的机制和病理生理学意义仍部分未知。研究表明，肥胖时脂肪组织缺氧，主要是由于脂肪细胞肥大导致炎症途径的过度激活。在动物和细胞模型中，缺氧诱导的炎症被证明会导致内分泌改变和代谢紊乱。然而，最近的证据表明，脂肪组织微血管可能受到一系列因素的调节，而不仅仅是简单的低氧理论，这些因素包括血管活性物质如血管紧张素 II、血管生成和糖化等。本文综述了这些因素在调节脂肪组织灌注中的作用以及脂肪组织微血管功能障碍的功能后果的最新知识。
