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Reduced Adipose Tissue Oxygenation in Human Obesity
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OBJECTIVE— Based on rodent studies, we examined the hypothesis that increased adipose tissue (AT) mass in obesity without an adequate support of vascularization might lead to hypoxia, macrophage infiltration, and inflammation. RESEARCH DESIGN AND METHODS— Oxygen partial pressure (AT pO2) and AT temperature in abdominal AT (9 lean and 12 overweight/obese men and women) was measured by direct insertion of a polarographic Clark electrode. Body composition was measured by dual-energy X-ray absorptiometry, and insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp. Abdominal subcutaneous tissue was used for staining, quantitative RT-PCR, and chemokine secretion assay. RESULTS— AT pO2 was lower in overweight/obese subjects than lean subjects (47 ± 10.6 vs. 55 ± 9.1 mmHg); however, this level of pO2 did not activate the classic hypoxia targets (pyruvate dehydrogenase kinase and vascular endothelial growth factor [VEGF]). AT pO2 was negatively correlated with percent body fat (R = −0.50, P < 0.05). Compared with lean subjects, overweight/obese subjects had 44% lower capillary density and 58% lower VEGF, suggesting AT rarefaction (capillary drop out). This might be due to lower peroxisome proliferator–activated receptor γ1 and higher collagen VI mRNA expression, which correlated with AT pO2 (P < 0.05). Of clinical importance, AT pO2 negatively correlated with CD68 mRNA and macrophage inflammatory protein 1α secretion (R = −0.58, R = −0.79, P < 0.05), suggesting that lower AT pO2 could drive AT inflammation in obesity. CONCLUSIONS— Adipose tissue rarefaction might lie upstream of both low AT pO2 and inflammation in obesity. These results suggest novel approaches to treat the dysfunctional AT found in obesity.
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“We observed a marked decrease in the proportion of capillary endothelial cells in eWAT specifically during HFD feeding, consistent with the previously documented capillary rarefaction and elevated hypoxia associated with adipose tissue expansion (Rosen and Spiegelman, 2014; Pasarica et al., 2009).”
From Robust single-nucleus RNA sequencing reveals depot-specific cell population dynamics in adipose tissue remodeling during obesity (2025) · cites this paper as Pasarica et al., 2009
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“For example, VEGF is upregulated in AT of mice fed a HFD for three days, but there are reports of both enhanced and reduced VEGF expression in chronic obesity (3,13,43,44), suggesting that sprouting angiogenesis is activated early and may or may not persist.”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [13]
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“Immune cells, particularly monocytes, migrate to areas of hypoxia, where they differentiate into proinflammatory macrophages (13,14).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [13]
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“Long-term HFF results in abnormal regulation of VEGF-A expression; not only do the VEGF-A levels decrease in the AT of obese mice and humans (13), but there is also evidence that the presence of VEGF in obese mice can block the regulation of neovascularization and vessel normalization (83).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [13]
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“Similar to findings in mice, human studies have reported that VEGF expression is reduced in obese humans (13).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [13]
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Metadata
- Authors
- Pasarica, M., Sereda, O. R., Redman, L. M., Albarado, D. C., Hymel, D. T., Roan, L. E., Rood, J. C., Burk, D. H., & Smith, S. R.
- Affiliations
- Pennington Biomedical Research Center (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2009-03-01
- Volume
- 58
- Issue
- 3
- Pages
- 718-725
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC2646071
- OpenAlex
- W2171965603
- Cited by
- 786
- References
- 46
- Citations by year
- 2026: 27 · 2025: 25 · 2024: 40 · 2023: 32 · 2022: 47 · 2021: 41 · 2020: 48 · 2019: 58 · 2018: 54 · 2017: 56 · 2016: 39 · 2015: 53 · 2014: 53 · 2013: 66 · 2012: 46
- FWCI
- 25.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Civil War Book Review (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK072476, P30DK072476)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- adipose tissue hypoxia, obesity, adipose tissue inflammation, macrophage infiltration, capillary density, vascular endothelial growth factor, PPARγ, collagen VI, CD68, macrophage inflammatory protein-1alpha, insulin sensitivity, adipose tissue vascularization
- MeSH terms
- Abdomen, Adipose Tissue, Hypoxia, Blood Pressure, Body Composition, Body Temperature, Female, Humans, Hyperinsulinism, Inflammation, Male, Obesity, Organ Size, Oxygen, Partial Pressure, Reference Values, Glucose Clamp Technique, Absorptiometry, Photon, Patient Selection, Reverse Transcriptase Polymerase Chain Reaction, Overweight
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