Oxford Centre for Diabetes, Endocrinology and Metabolism (OCDEM); University of Oxford; Oxford, UK.
Adipocyte. 2014 Jan 1;3(1):75-80. doi: 10.4161/adip.27114. Epub 2013 Nov 13.
With the increasing prevalence of obesity there is a concomitant increase in white adipose tissue dysfunction, with the tissue moving toward a proinflammatory phenotype. Adipose tissue hypoxia has been proposed as a key underlying mechanism triggering tissue dysfunction but data from human, in vivo studies, to support this hypothesis is limited. Human adipose tissue oxygenation has been investigated by direct assessment of tissue oxygen tension (pO2) or by expression of hypoxia-sensitive genes/protein in lean and obese subjects but findings are inconsistent. An obvious read-out of hypoxia is the effect on intermediary metabolism, and we have investigated the functional consequences, in terms of a "metabolic signature" of human adipose tissue hypoxia in vivo. Here, we discuss the different approaches used and the importance of integrative physiological techniques to try and elucidate what defines adipose tissue hypoxia in humans.
随着肥胖症的发病率不断上升，白色脂肪组织功能障碍也随之增加，组织向促炎表型转变。脂肪组织缺氧被认为是触发组织功能障碍的关键潜在机制，但支持这一假说的人体、体内研究数据有限。人们通过直接评估组织氧分压（pO2）或在瘦人和肥胖受试者中检测缺氧敏感基因/蛋白来研究人体脂肪组织的氧合作用，但研究结果并不一致。缺氧的一个明显表现是对中间代谢的影响，我们已经研究了体内人类脂肪组织缺氧的“代谢特征”的功能后果。在这里，我们讨论了所使用的不同方法以及综合生理学技术的重要性，以试图阐明在人类中定义脂肪组织缺氧的因素。
