Adapting to obesity with adipose tissue inflammation
Abstract
Adipose tissue not only has an important role in the storage of excess nutrients but also senses nutrient status and regulates energy mobilization. An overall positive energy balance is associated with overnutrition and leads to excessive accumulation of fat in adipocytes. These cells respond by initiating an inflammatory response that, although maladaptive in the long run, might initially be a physiological response to the stresses obesity places on adipose tissue. In this Review, we characterize adipose tissue inflammation and review the current knowledge of what triggers obesity-associated inflammation in adipose tissue. We examine the connection between adipose tissue inflammation and the development of insulin resistance and catecholamine resistance and discuss the ensuing state of metabolic inflexibility. Finally, we review the current and potential new anti-inflammatory treatments for obesity-associated metabolic disease.
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M1 macrophages secrete TNF-α, IL-1β, IL-6, and chemokines that promote the influx of activated CD4+ Th1 cells.
“M1 macrophages secrete TNF-α, IL-1β, IL-6, and chemokines that promote the influx of activated CD4+ Th1 cells [14,20,239,248].”
The β3-adrenergic receptor downstream signaling pathway may be attenuated in obesity by chronic TNF-α exposure through NF-κB-mediated upregulation of IKKε and TBK1, which inhibit cAMP signaling via phosphodiesterase 3B.
“Its downstream signaling pathway may be attenuated in obesity by chronic exposure to TNF-α through NF-κB-mediated upregulation of IKKε and TBK1, which inhibit cAMP signaling via phosphodiesterase 3B [239].”
Low-grade chronic inflammation associated with obesity may be one mechanistic link between AGEs and insulin resistance.
“he low-grade chronic inflammation associated with obesity may be one of the mechanistic links between AGEs and insulin resistance.[118,119]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [118]
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References 180 · Cited by 1,204
- Authors
- Reilly, S. M., & Saltiel, A. R.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Saltiel, Alan R.
- Venue
- Nature Reviews Endocrinology
- Published
- 2017-08-11
- Volume
- 13
- Issue
- 11
- Pages
- 633-643
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- OpenAlex
- W2743155225
- Cited by
- 1,204
- References
- 180
- Citations by year
- 2026: 91 · 2025: 96 · 2024: 145 · 2023: 138 · 2022: 181 · 2021: 179 · 2020: 166 · 2019: 113 · 2018: 83 · 2017: 9
- FWCI
- 13.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (K01DK105075, P30DK063491)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- adipose tissue inflammation, obesity, overnutrition, insulin resistance, catecholamine resistance, metabolic inflexibility, adipocytes, energy balance, anti-inflammatory therapy
- MeSH terms
- Adaptation, Physiological, Adipose Tissue, Catecholamines, Energy Metabolism, Homeostasis, Humans, Immunity, Innate, Inflammation, Insulin Resistance, Obesity, Adipocytes, Overnutrition
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