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Cited by 1,186Adipokines, Inflammation, and Metabolic DiseasesCardiovascular Disease and AdiposityAdipose Tissue and Metabolism

The DOI matches its Crossref record; 122 of the 124 references it cites were found in a registry or an index.

Chronic Inflammation in Obesity and the Metabolic Syndrome

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Monteiro, Rosário, Azevedo, Isabel·2010·Mediators of Inflammation
DOI 10.1155/2010/289645PMC PMC2913796
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Abstract

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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Figure 1 Overview of the complex interplay between obesity-inflammation-metabolic syndrome: metabolic overload impacts on adipose tissue, leading to organelle stress with production of ROS and adipokines, as well as activation of kinases that potentiate the transcription of inflammatory genes and interfere with insulin signaling. Hyperthrophy facilitates rupture of adipocytes which attract and activate macrophages that markedly reinforce the inflammatory process through further production of ROS and inflammatory cytokines. Production of adiponectin, an anti-inflammatory cytokine, is reduced. Increase of FFA concentration, namely, SFA, coming both from feeding and adipose tissue overflow, accumulates in the liver, among other organs. Fat accumulation in the liver leads to overproduction of LDLs and, together with IL-6, of CRP. NAFLD is a frequent consequence of these metabolic dysregulations, and all this impacts on insulin sensitivity. SFA activates TOLL-like receptors in adipocytes, contributing to the activation of the inflammatory response. Fat has also effects on intestinal permeability and on the microbiota, with systemic inflammatory consequences. Most excess metabolites and cytokines produced throughout these processes converge on insulin resistance, a central characteristic of the metabolic syndrome. AP-1: activator protein-1; CRP: C-reactive protein; FFA: free (nonesterified) fatty acids; IL-n: interleukins; IKK: inhibitor of NF-κB kinase; IL-6: interleukin-6; Int: intestine; IR: insulin resistance; JNK: c-Jun N-terminal kinase; LDL: low density lipoprotein; M: microbiota; NAFLD: nonalcoholic fatty liver disease; NF-κB: nuclear factor κB; OxS: oxidative stress; ROS: reactive oxygen species; PKC: protein kinase C; SFA: saturated fatty acids; TAG: triacylglycerols; TLR: TOLL-like receptors; TNFalpha: tumour necrosis factor alpha.
Figure 1 Overview of the complex interplay between obesity-inflammation-metabolic syndrome: metabolic overload impacts on adipose tissue, leading to organelle stress with production of ROS and adipokines, as well as activation of kinases that potentiate the transcription of inflammatory genes and interfere with insulin signaling. Hyperthrophy facilitates rupture of adipocytes which attract and activate macrophages that markedly reinforce the inflammatory process through further production of ROS and inflammatory cytokines. Production of adiponectin, an anti-inflammatory cytokine, is reduced. Increase of FFA concentration, namely, SFA, coming both from feeding and adipose tissue overflow, accumulates in the liver, among other organs. Fat accumulation in the liver leads to overproduction of LDLs and, together with IL-6, of CRP. NAFLD is a frequent consequence of these metabolic dysregulations, and all this impacts on insulin sensitivity. SFA activates TOLL-like receptors in adipocytes, contributing to the activation of the inflammatory response. Fat has also effects on intestinal permeability and on the microbiota, with systemic inflammatory consequences. Most excess metabolites and cytokines produced throughout these processes converge on insulin resistance, a central characteristic of the metabolic syndrome. AP-1: activator protein-1; CRP: C-reactive protein; FFA: free (nonesterified) fatty acids; IL-n: interleukins; IKK: inhibitor of NF-κB kinase; IL-6: interleukin-6; Int: intestine; IR: insulin resistance; JNK: c-Jun N-terminal kinase; LDL: low density lipoprotein; M: microbiota; NAFLD: nonalcoholic fatty liver disease; NF-κB: nuclear factor κB; OxS: oxidative stress; ROS: reactive oxygen species; PKC: protein kinase C; SFA: saturated fatty acids; TAG: triacylglycerols; TLR: TOLL-like receptors; TNFalpha: tumour necrosis factor alpha.CC BY · PubMed Central

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Cites

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Research works printed but not linked: 5

  1. 2003, Endocrine Practice, 9, 237
  2. 2000, Journal of Clinical Endocrinology and Metabolism, 85, 3338
  3. 2000, Diabetes and Metabolism, 26, 178
  4. 2008, International Journal of Obesity, 32, S11
  5. 2006, Journal of the American College of Nutrition, 25, 262S

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Metadata

Authors
Monteiro, R., & Azevedo, I.
Affiliations
Universidade do Porto (PT)
Corresponding author
Monteiro, Rosário
ORCID
Venue
Mediators of Inflammation
Publisher
Wiley
Published
2010
Volume
2010
Pages
1-10
ISSN
  • 0962-9351 (ISSN-L)
  • 1466-1861
DOI
10.1155/2010/289645
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
Licence
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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