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...
| Hauptverfasser: | , , , |
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| Format: | Journal article |
| Sprache: | English |
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2013
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| _version_ | 1826293242588561408 |
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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. |
| first_indexed | 2024-03-07T03:27:05Z |
| format | Journal article |
| id | oxford-uuid:b96d1039-36a8-4976-995c-73f3dc0fc6d8 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T03:27:05Z |
| publishDate | 2013 |
| record_format | dspace |
| 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 |