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 O₂ tension; the obvious read out of hypoxia...

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मुख्य लेखकों: Hodson, L, Humphreys, S, Karpe, F, Frayn, K
स्वरूप: Journal article
भाषा:English
प्रकाशित: 2013
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author Hodson, L
Humphreys, S
Karpe, F
Frayn, K
author_facet Hodson, L
Humphreys, S
Karpe, F
Frayn, K
author_sort Hodson, L
collection OXFORD
description 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 O₂ 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. O₂ delivery to AT was reduced in obesity (P < 0.05). However, O₂ 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 O₂ to the obese AT is reduced, O₂ consumption is low, and metabolic signatures of human AT do not support the notion of a hypoxic state in obesity.
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spelling oxford-uuid:b96d1039-36a8-4976-995c-73f3dc0fc6d82022-03-27T05:02:43ZMetabolic signatures of human adipose tissue hypoxia in obesity.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:b96d1039-36a8-4976-995c-73f3dc0fc6d8EnglishSymplectic Elements at Oxford2013Hodson, LHumphreys, SKarpe, FFrayn, KAdipose 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 O₂ 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. O₂ delivery to AT was reduced in obesity (P < 0.05). However, O₂ 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 O₂ to the obese AT is reduced, O₂ consumption is low, and metabolic signatures of human AT do not support the notion of a hypoxic state in obesity.
spellingShingle Hodson, L
Humphreys, S
Karpe, F
Frayn, K
Metabolic signatures of human adipose tissue hypoxia in obesity.
title Metabolic signatures of human adipose tissue hypoxia in obesity.
title_full Metabolic signatures of human adipose tissue hypoxia in obesity.
title_fullStr Metabolic signatures of human adipose tissue hypoxia in obesity.
title_full_unstemmed Metabolic signatures of human adipose tissue hypoxia in obesity.
title_short Metabolic signatures of human adipose tissue hypoxia in obesity.
title_sort metabolic signatures of human adipose tissue hypoxia in obesity
work_keys_str_mv AT hodsonl metabolicsignaturesofhumanadiposetissuehypoxiainobesity
AT humphreyss metabolicsignaturesofhumanadiposetissuehypoxiainobesity
AT karpef metabolicsignaturesofhumanadiposetissuehypoxiainobesity
AT fraynk metabolicsignaturesofhumanadiposetissuehypoxiainobesity