Journal
DIABETES
Volume 62, Issue 5, Pages 1417-1425Publisher
AMER DIABETES ASSOC
DOI: 10.2337/db12-1032
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Funding
- Wellcome Trust (U.K.)
- New Zealand Health Research Council
- Girdlers' Company (U.K.)
- Food Standards Agency (U.K.)
- British Heart Foundation (U.K.)
- British Heart Foundation [FS/11/18/28633] Funding Source: researchfish
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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-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-2 delivery to AT was reduced in obesity (P < 0.05). However, O-2 consumption was low (<30% of resting forearm skeletal muscle [SM], P < 0.001); this was not related to obesity. AT primarily oxidized glucose, as demonstrated by a respiratory quotient close to 1.0 (higher than SM, P < 0.05). AT was a net producer of lactate, but there was an inverse relationship in venous outflow between lactate-to-pyruvate ratio (a marker of cytosolic redox state) and BMI, suggesting that AT is glycolytic but obese AT is not hypoxic. Although delivery of O-2 to the obese AT is reduced, 02 consumption is low, and metabolic signatures of human AT do not support the notion of a hypoxic state in obesity. Diabetes 62:1417-1425, 2013
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