Adipose tissue, adipokines, and inflammation
Abstract
White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-alpha, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.
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Altering any health behaviors leads to a reduction in the risk factors for preventable non-communicable diseases.
“Even if it is well understood that altering any health behaviors leads to a reduction in the risk factors for preventable non-communicable diseases [18,20,26-33].”
The greatest impact of these endocrinological changes appears related to alterations in sex hormones (testosterone and androgens), growth hormone, and adipokines.
“The greatest impact of these changes appears to be related to alterations in sex hormone (i.e. testosterone and androgens), growth hormone, and a host of adipokines [29,34-46].”
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Self-citationMaternal Obesity in Pregnancy, Gestational Weight Gain, and Risk of Childhood Asthma
Forno, E., Young, O. M., Kumar, R., Simhan, H. N., & Celedon, J. C. (2014) · PEDIATRICS · doi:10.1542/peds.2014-0439 · Cited by 230 · see citing works
- Authors
- Fantuzzi, G.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Fantuzzi, Giamila
- ORCID
- Fantuzzi, Giamila
- Venue
- Journal of Allergy and Clinical Immunology
- Publisher
- Elsevier BV
- Published
- 2005-05
- Volume
- 115
- Issue
- 5
- Pages
- 911-919
- ISSN
- 0091-6749 (ISSN-L)
- OpenAlex
- W2158079900
- Cited by
- 2,606
- References
- 89
- Citations by year
- 2026: 45 · 2025: 67 · 2024: 96 · 2023: 117 · 2022: 119 · 2021: 127 · 2020: 112 · 2019: 121 · 2018: 123 · 2017: 145 · 2016: 112 · 2015: 132 · 2014: 139 · 2013: 184 · 2012: 148
- FWCI
- 16.18
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Allergy and Clinical Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK061483, DK-061483)
- 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
- white adipose tissue, adipokines, inflammation, adipose tissue macrophages, leptin, adiponectin, resistin, visfatin, TNF-α, interleukin-6, MCP-1, insulin resistance, obesity, cardiovascular disease, infection susceptibility, T cell response, malnutrition
- MeSH terms
- Adipose Tissue, Animals, Autoimmune Diseases, Hormones, Ectopic, Humans, Inflammation, Insulin Resistance, Macrophages, Obesity, Complement Factor D, Serine Endopeptidases, Cytokines, Adipocytes, Leptin, Intercellular Signaling Peptides and Proteins, Adiponectin, Resistin, Nicotinamide Phosphoribosyltransferase
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