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Cited by 786Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

Reduced Adipose Tissue Oxygenation in Human Obesity

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Pasarica, Magdalena, Sereda, Olga R., Redman, Leanne M., Albarado, Diana C., Hymel, David T., Roan, Laura E., Rood, Jennifer C., Burk, David H. +1 more·2009·Diabetes
DOI 10.2337/db08-1098PMC PMC2646071
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Abstract

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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  • They 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.

    “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

  • VEGF is upregulated in adipose tissue of mice fed a high-fat diet for three days, but reports in chronic obesity show both enhanced and reduced VEGF expression.

    “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]

  • Monocytes migrate to hypoxic areas and differentiate into proinflammatory macrophages.

    “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]

  • Long-term high-fat feeding results in abnormal regulation of VEGF-A expression, with decreased VEGF-A levels in adipose tissue of obese mice and humans.

    “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]

  • Human studies have reported lower VEGF expression in obese humans, matching findings in mice.

    “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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Research works printed but not linked: 1

  1. [1]Smith SR, Ravussin E: Role of Adipocyte in Metabolism and Endocrine Function. DeGroot, Jameson, Endocrinology, Philadelphia, Elsevier Saunders, 2006

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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)
ORCID
Venue
Diabetes
Publisher
American Diabetes Association
Published
2009-03-01
Volume
58
Issue
3
Pages
718-725
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
DOI
10.2337/db08-1098
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
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 › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › 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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