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Obesity, inflammation and the immune system
Open accessAbstract
Obesity shares with most chronic diseases the presence of an inflammatory component, which accounts for the development of metabolic disease and other associated health alterations. This inflammatory state is reflected in increased circulating levels of pro-inflammatory proteins, and it occurs not only in adults but also in adolescents and children. The chronic inflammatory response has its origin in the links existing between the adipose tissue and the immune system. Obesity, like other states of malnutrition, is known to impair the immune function, altering leucocyte counts as well as cell-mediated immune responses. In addition, evidence has arisen that an altered immune function contributes to the pathogenesis of obesity. This review attempts to briefly comment on the various plausible explanations that have been proposed for the phenomenon: (1) the obesity-associated increase in the production of leptin (pro-inflammatory) and the reduction in adiponectin (anti-inflammatory) seem to affect the activation of immune cells; (2) NEFA can induce inflammation through various mechanisms (such as modulation of adipokine production or activation of Toll-like receptors); (3) nutrient excess and adipocyte expansion trigger endoplasmic reticulum stress; and (4) hypoxia occurring in hypertrophied adipose tissue stimulates the expression of inflammatory genes and activates immune cells. Interestingly, data suggest a greater impact of visceral adipose tissue and central obesity, rather than total body fat, on the inflammatory process. In summary, there is a positive feedback loop between local inflammation in adipose tissue and altered immune response in obesity, both contributing to the development of related metabolic complications.
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“Long‐time stress appears to also contribute to pathogenesis of other sepsis comorbidities including obesity, diabetes, asthma and immunosenescence (de Heredia et al., 2012; Epel et al., 2004; Epel et al., 2008; Rod et al., 2012; Thakur et al., 2017).”
From On race, human variation, and who gets and dies of sepsis (2022) · cites this paper as de Heredia et al., 2012
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“CMV reactivation might be even more frequent in obesity, because excess adiposity drives chronic systemic inflammation and oxidative stress (Aroor and DeMarco 2014; Cervellati et al. 2014; de Heredia et al. 2012; Kanneganti and Dixit 2012; Le Lay and Simard 2014), which in turn can reactivate CMV directly (Cinatl et al. 1999; Docke et al. 1994; Jaganjac et al. 2010; Prosch et al. 1995; Speir 2000;”
From Is immunosenescence influenced by our lifetime “dose” of exercise? (2016) · cites this paper as de Heredia et al. 2012
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Metadata
- Authors
- de Heredia, F. P., Gómez-Martínez, S., & Marcos, A.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Venue
- Proceedings of the Nutrition Society
- Publisher
- Cambridge University Press (CUP)
- Published
- 2012-03-20
- Volume
- 71
- Issue
- 2
- Pages
- 332-338
- ISSN
- 0029-6651 (ISSN-L)
- 1475-2719
- OpenAlex
- W2001652786
- Cited by
- 845
- References
- 52
- Citations by year
- 2026: 32 · 2025: 97 · 2024: 87 · 2023: 94 · 2022: 92 · 2021: 86 · 2020: 65 · 2019: 47 · 2018: 44 · 2017: 35 · 2016: 39 · 2015: 37 · 2014: 39 · 2013: 40 · 2012: 10
- FWCI
- 5.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of The Nutrition Society (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, other-oa)
- 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
- obesity, chronic inflammation, leptin, adiponectin, free fatty acids, Toll-like receptors, adipokines, endoplasmic reticulum stress, hypoxia, visceral adipose tissue, abdominal obesity, immune function, metabolic disorders, children and adolescents
- MeSH terms
- Adipose Tissue, Hypoxia, Endoplasmic Reticulum, Fatty Acids, Humans, Immune System, Inflammation, Obesity, Overnutrition, Adipokines, Endoplasmic Reticulum Stress
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