The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Abdominal adipose tissue cytokine gene expression: relationship to obesity and metabolic risk factors
Abstract
Adipose tissue is a major source of inflammatory and thrombotic cytokines. This study investigated the relationship of abdominal subcutaneous adipose tissue cytokine gene expression to body composition, fat distribution, and metabolic risk during obesity. We determined body composition, abdominal fat distribution, plasma lipids, and abdominal subcutaneous fat gene expression of leptin, TNF-α, IL-6, PAI-1, and adiponectin in 20 obese, middle-aged women (BMI, 32.7 ± 0.8 kg/m 2; age, 57 ± 1 yr). A subset of these women without diabetes ( n = 15) also underwent an OGTT. In all women, visceral fat volume was negatively related to leptin ( r = −0.46, P < 0.05) and tended to be negatively related to adiponectin ( r = −0.38, P = 0.09) gene expression. Among the nondiabetic women, fasting insulin ( r = 0.69, P < 0.01), 2-h insulin ( r = 0.56, P < 0.05), and HOMA index ( r = 0.59, P < 0.05) correlated positively with TNF-α gene expression; fasting insulin ( r = 0.54, P < 0.05) was positively related to, and 2-h insulin ( r = 0.49, P = 0.06) tended to be positively related to, IL-6 gene expression; and glucose area ( r = −0.56, P < 0.05) was negatively related to, and insulin area ( r = −0.49, P = 0.06) tended to be negatively related to, adiponectin gene expression. Also, adiponectin gene expression was significantly lower in women with vs. without the metabolic syndrome (adiponectin-β-actin ratio, 2.26 ± 0.46 vs. 3.31 ± 0.33, P < 0.05). We conclude that abdominal subcutaneous adipose tissue expression of inflammatory cytokines is a potential mechanism linking obesity with its metabolic comorbidities.
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“In the presence of obesity, adipose tissue indeed produces cytokines in excess, whereas output of adiponectin is diminished; these responses appear to heighten the connection between obesity and inflammation.35”
From Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement (2005) · cites this paper as [35]
In the citing paper
“These include increased production of inflammatory cytokines, 35,36 plasminogen activator inhibitor-1, 37 and other bioactive products 38 -40 ; at the same time the potentially protective adipokine, adiponectin, is reduced.41,42”
From Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement (2005) · cites this paper as [35]
In the citing paper
“In addition, a large number of studies have been carried out to evaluate the ATP III criteria for the metabolic syndrome.35, The majority of these reports are supportive of the present structure of ATP III criteria.”
From Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement (2005) · cites this paper as [35]
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Metadata
- Authors
- You, T., Yang, R., Lyles, M. F., Gong, D., & Nicklas, B. J.
- Affiliations
- Wake Forest University Health Sciences (US)
- Venue
- American Journal of Physiology-Endocrinology and Metabolism
- Publisher
- American Physiological Society
- Published
- 2005-04
- Volume
- 288
- Issue
- 4
- Pages
- E741-E747
- ISSN
- 0193-1849 (ISSN-L)
- 1522-1555
- OpenAlex
- W2120159188
- Cited by
- 173
- References
- 45
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 2 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 4 · 2019: 7 · 2018: 4 · 2017: 2 · 2016: 7 · 2015: 5 · 2014: 9 · 2013: 5 · 2012: 10
- FWCI
- 10.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Wake Forest University
- Wake Forest School of Medicine
- National Institute on Aging (R01-AG/DK20583, P30AG-21332, P30AG021332)
- National Center for Research Resources (M01RR-07122, M01RR007122)
- NIH Clinical Center
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- subcutaneous abdominal fat, cytokine gene expression, obesity, metabolic syndrome, leptin, adiponectin, TNF-α, interleukin-6, plasminogen activator inhibitor-1, visceral fat, insulin resistance, HOMA index, glucose tolerance, middle-aged women, adipose tissue inflammation
- MeSH terms
- Abdomen, Adipose Tissue, Aged, Blood Glucose, Body Composition, Female, Gene Expression Regulation, Glucose Tolerance Test, Humans, Insulin, Cholesterol, HDL, Middle Aged, Obesity, Triglycerides, Tumor Necrosis Factor-alpha, Exercise, Absorptiometry, Photon, Interleukin-6, Cytokines, Plasminogen Activator Inhibitor 1, Leptin, Metabolic Syndrome, Intercellular Signaling Peptides and Proteins, Adiponectin
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