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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.

Original publication




Journal article



Publication Date





75 - 80


adipose tissue, human, hypoxia, metabolic signatures, metabolism, oxygen tension