Chronic tissue inflammation and metabolic disease

Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely recognized that chronic, subacute tissue inflammation is a major etiologic component of the pathogenesis of insulin resistance and metabolic...

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Published inGenes & development Vol. 35; no. 5-6; pp. 307 - 328
Main Authors Lee, Yun Sok, Olefsky, Jerrold
Format Journal Article
LanguageEnglish
Published United States Cold Spring Harbor Laboratory Press 01.03.2021
Subjects
Review
metaflammation
β-cell dysfunction
immunometabolism
inflammation
glucose intolerance
macrophage
insulin resistance
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Abstract Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely recognized that chronic, subacute tissue inflammation is a major etiologic component of the pathogenesis of insulin resistance and metabolic dysfunction in obesity. Here, we summarize recent advances in our understanding of immunometabolism. We discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events, including a focus on the role of adipose tissue hypoxia and macrophage-derived exosomes. Last, we also review current and potential new therapeutic strategies based on immunomodulation.
AbstractList Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely recognized that chronic, subacute tissue inflammation is a major etiologic component of the pathogenesis of insulin resistance and metabolic dysfunction in obesity. Here, we summarize recent advances in our understanding of immunometabolism. We discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events, including a focus on the role of adipose tissue hypoxia and macrophage-derived exosomes. Last, we also review current and potential new therapeutic strategies based on immunomodulation.
In this review, Lee and Olefsky discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events, including a focus on the role of adipose tissue hypoxia and macrophage-derived exosomes. Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely recognized that chronic, subacute tissue inflammation is a major etiologic component of the pathogenesis of insulin resistance and metabolic dysfunction in obesity. Here, we summarize recent advances in our understanding of immunometabolism. We discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events, including a focus on the role of adipose tissue hypoxia and macrophage-derived exosomes. Last, we also review current and potential new therapeutic strategies based on immunomodulation.
Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely recognized that chronic, subacute tissue inflammation is a major etiologic component of the pathogenesis of insulin resistance and metabolic dysfunction in obesity. Here, we summarize recent advances in our understanding of immunometabolism. We discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events, including a focus on the role of adipose tissue hypoxia and macrophage-derived exosomes. Last, we also review current and potential new therapeutic strategies based on immunomodulation.Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely recognized that chronic, subacute tissue inflammation is a major etiologic component of the pathogenesis of insulin resistance and metabolic dysfunction in obesity. Here, we summarize recent advances in our understanding of immunometabolism. We discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events, including a focus on the role of adipose tissue hypoxia and macrophage-derived exosomes. Last, we also review current and potential new therapeutic strategies based on immunomodulation.
Author Lee, Yun Sok
Olefsky, Jerrold
AuthorAffiliation Department of Medicine, Division of Endocrinology and Metabolism, University of California at San Diego, La Jolla, California 92093, USA
AuthorAffiliation_xml – name: Department of Medicine, Division of Endocrinology and Metabolism, University of California at San Diego, La Jolla, California 92093, USA
Author_xml – sequence: 1
  givenname: Yun Sok
  orcidid: 0000-0001-7967-4734
  surname: Lee
  fullname: Lee, Yun Sok
– sequence: 2
  givenname: Jerrold
  surname: Olefsky
  fullname: Olefsky, Jerrold
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33649162$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2021 Lee and Olefsky; Published by Cold Spring Harbor Laboratory Press.
2021
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Keywords metaflammation
β-cell dysfunction
immunometabolism
inflammation
glucose intolerance
macrophage
insulin resistance
Language English
License 2021 Lee and Olefsky; Published by Cold Spring Harbor Laboratory Press.
This article, published in Genes & Development, is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.
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Snippet Obesity is the most common cause of insulin resistance, and the current obesity epidemic is driving a parallel rise in the incidence of T2DM. It is now widely...
In this review, Lee and Olefsky discuss the characteristics of chronic inflammation in the major metabolic tissues and how obesity triggers these events,...
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SubjectTerms Review
Title Chronic tissue inflammation and metabolic disease
URI https://www.ncbi.nlm.nih.gov/pubmed/33649162
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https://pubmed.ncbi.nlm.nih.gov/PMC7919414
Volume 35
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