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Chronic Inflammation in Obesity and the Metabolic Syndrome
Open accessAbstract
The increasing incidence of obesity and the metabolic syndrome is disturbing. The activation of inflammatory pathways, used normally as host defence, reminds the seriousness of this condition. There is probably more than one cause for activation of inflammation. Apparently, metabolic overload evokes stress reactions, such as oxidative, inflammatory, organelle and cell hypertrophy, generating vicious cycles. Adipocyte hypertrophy, through physical reasons, facilitates cell rupture, what will evoke an inflammatory reaction. Inability of adipose tissue development to engulf incoming fat leads to deposition in other organs, mainly in the liver, with consequences on insulin resistance. The oxidative stress which accompanies feeding, particularly when there is excessive ingestion of fat and/or other macronutrients without concomitant ingestion of antioxidant-rich foods/beverages, may contribute to inflammation attributed to obesity. Moreover, data on the interaction of microbiota with food and obesity brought new hypothesis for the obesity/fat diet relationship with inflammation. Beyond these, other phenomena, for instance psychological and/or circadian rhythm disturbances, may likewise contribute to oxidative/inflammatory status. The difficulty in the management of obesity/metabolic syndrome is linked to their multifactorial nature where environmental, genetic and psychosocial factors interact through complex networks.
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“Continuous low-level translocation of LPS into circulation can induce chronic low-level inflammatory states associated with development of obesity and other metabolic syndromes [92].”
From The athletic gut microbiota (2020) · cites this paper as [92]
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“As systemic inflammatory markers 123 and metabolites such as those derived from the gut microbiota have been associated with obesity and food addiction, future mechanistic studies that integrate these mediators are also of value.”
From History of early life adversity is associated with increased food addiction and sex-specific alterations in reward network connectivity in obesity (2019) · cites this paper as [123]
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“Since these disorders share a mechanistic origin involving inflammation (Levy, 2009; Lee and Giuliani, 2019; Martinez et al., 2018; Steven, 2019; Kaunzner, 2019; Monteiro and Azevedo, 2010), it has been proposed that ELA-driven changes in the immune system are the root underlying susceptibility to these diseases.”
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“Adipose tissue, then, significantly contributes to systemic inflammatory processes [20,21] and to insulin resistance and hyperinsulinemia.”
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“chronic state of low-grade inflammation (44, 45), which in turn has been associatedwithmethylation (46).”
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“Inflammation is commonly seen in all obesity and diabetic humans and in animal models that can be primarily initiated by nutrient overload [35].”
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“Metabolic overload can initiate the oxidative stress, and thus contribute to the onset of chronic inflammation triggering to a cascade of molecular reactions that leads to cellular dysfunction [9].”
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“As it is not accompanied by infection or massive tissue injury, it is often termed ‘low‑grade’ chronic inflammation (2).”
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“Inflammatory markers, including C-reactive protein, interleukin-6, and tumor necrosis factor, are positively related to obesity and the aggravation of insulin resistance [37].”
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Metadata
- Authors
- Monteiro, R., & Azevedo, I.
- Affiliations
- Universidade do Porto (PT)
- Corresponding author
- Monteiro, Rosário
- Venue
- Mediators of Inflammation
- Publisher
- Wiley
- Published
- 2010
- Volume
- 2010
- Pages
- 1-10
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC2913796
- OpenAlex
- W1997248937
- Cited by
- 1,186
- References
- 124
- Citations by year
- 2026: 40 · 2025: 93 · 2024: 104 · 2023: 99 · 2022: 126 · 2021: 102 · 2020: 120 · 2019: 113 · 2018: 95 · 2017: 68 · 2016: 47 · 2015: 33 · 2014: 29 · 2013: 45 · 2012: 34
- FWCI
- 4.15
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- 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
- obesity, metabolic syndrome, chronic inflammation, adipocyte hypertrophy, oxidative stress, insulin resistance, hepatic lipid accumulation, gut microbiota, dietary fat, circadian rhythm, psychological factors, adipose tissue
- MeSH terms
- Animals, Energy Metabolism, Humans, Inflammation, Obesity, Adipocytes, Metabolic Syndrome
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