Metabolic signatures of human adipose tissue hypoxia in obesity

Adipose tissue (AT) hypoxia has been proposed as the cause of obesity-related AT dysfunction, moving the tissue toward a proinflammatory phenotype. In humans, AT oxygenation has been assessed by expression of hypoxia-sensitive genes or direct assessment of [O.sub.2] tension; the obvious read out of hypoxia, effects on intermediary metabolism, has not been investigated. We used tissue-specific venous catheterization of subcutaneous abdominal AT in humans to investigate oxygen-related metabolic processes, searching for metabolic signatures relating to hypoxia in obesity. [O.sub.2] delivery to AT was reduced in obesity (P < 0.05). However, [O.sub.2] consumption was low (
Subcutaneous adipose tissue (SCAT) is a complex metabolic organ that responds dynamically to alterations in nutritional state. As the tissue expands, macrophages infiltrate and orchestrate inflammatory responses via molecules such [...]