The DOI matches its Crossref record; 51 of the 52 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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
Experimental — accuracy not yet measuredIn the citing paper
“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
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Obesity is associated with macrophage accumulation in adipose tissue
Weisberg, S. P., McCann, D., Desai, M., Rosenbaum, M., Leibel, R. L., & Ferrante, A. W. (2003) · Journal of Clinical Investigation · doi:10.1172/jci200319246 · Cited by 10,041
Inflammation and metabolic disorders
Hotamisligil, G. S. (2006) · Nature · doi:10.1038/nature05485 · Cited by 9,199
Obesity induces a phenotypic switch in adipose tissue macrophage polarization
Lumeng, C. N., Bodzin, J. L., & Saltiel, A. R. (2007) · Journal of Clinical Investigation · doi:10.1172/jci29881 · Cited by 4,664
Obesity and the Metabolic Syndrome in Children and Adolescents
Weiss, R., Dziura, J., Burgert, T. S., Tamborlane, W. V., Taksali, S. E., Yeckel, C. W., Allen, K., Lopes, M., Savoye, M., Morrison, J. A., et al. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa031049 · Cited by 3,495
Adipocytokines: mediators linking adipose tissue, inflammation and immunity
Tilg, H., & Moschen, A. R. (2006) · Nature reviews. Immunology · doi:10.1038/nri1937 · Cited by 3,272
Subcutaneous and visceral adipose tissue: their relation to the metabolic syndrome
Wajchenberg, B. L. (2000) · Endocrine Reviews · doi:10.1210/edrv.21.6.0415 · Cited by 2,961
Adipokines: inflammation and the pleiotropic role of white adipose tissue
Trayhurn, P., & Wood, I. S. (2004) · British Journal of Nutrition · doi:10.1079/bjn20041213 · Cited by 2,210
Macrophage-specific PPARγ controls alternative activation and improves insulin resistance
Odegaard, J. I., Ricardo-Gonzalez, R. R., Goforth, M. H., Morel, C. R., Subramanian, V., Mukundan, L., Eagle, A. R., Vats, D., Brombacher, F., Ferrante, A. W., et al. (2007) · Nature · doi:10.1038/nature05894 · Cited by 2,107
Recent advances in the relationship between obesity, inflammation, and insulin resistance.
Bastard, J., Maachi, M., Lagathu, C., Kim, M. J., Caron, M., Vidal, H., Capeau, J., & Fève, B. (2006) · PubMed · Cited by 2,090
Adipose tissue expandability, lipotoxicity and the Metabolic Syndrome — An allostatic perspective
Virtue, S., & Vidal-Puig, A. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2009.12.006 · Cited by 1,013
Research works printed but not linked: 2
- Gorman, 2004, Health: the fires within, Time, 163, 38
- Pérez de Heredia, 2010, Lactate enhances the inflammatory response in human preadipocytes in vitro, Obes Rev, 11, 122
Cited by
Sorted by citations
So depression is an inflammatory disease, but where does the inflammation come from?
Berk, M., Williams, L. J., Jacka, F. N., O’Neil, A., Pasco, J. A., Moylan, S., Allen, N. B., Stuart, A. L., Hayley, A. C., Byrne, M. L., et al. (2013) · BMC Medicine · doi:10.1186/1741-7015-11-200 · Cited by 1,423
Early Developmental Conditioning of Later Health and Disease: Physiology or Pathophysiology?
Hanson, M. A., & Gluckman, P. D. (2014) · Physiological Reviews · doi:10.1152/physrev.00029.2013 · Cited by 1,188
González‐Muniesa, P., Martínez‐González, M. Á., Hu, F. B., Després, J., Matsuzawa, Y., Loos, R. J. F., Moreno, L. A., Bray, G. A., & Martínez, J. A. (2017) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2017.34 · Cited by 1,184
Palaiodimos, L., Kokkinidis, D. G., Li, W., Karamanis, D., Ognibene, J., Arora, S., Southern, W. N., & Mantzoros, C. S. (2020) · Metabolism · doi:10.1016/j.metabol.2020.154262 · Cited by 864
Kuo, M. (2015) · Frontiers in Psychology · doi:10.3389/fpsyg.2015.01093 · Cited by 900
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
