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Inflammatory mechanisms linking obesity and metabolic disease
Open accessAbstract
There are currently over 1.9 billion people who are obese or overweight, leading to a rise in related health complications, including insulin resistance, type 2 diabetes, cardiovascular disease, liver disease, cancer, and neurodegeneration. The finding that obesity and metabolic disorder are accompanied by chronic low-grade inflammation has fundamentally changed our view of the underlying causes and progression of obesity and metabolic syndrome. We now know that an inflammatory program is activated early in adipose expansion and during chronic obesity, permanently skewing the immune system to a proinflammatory phenotype, and we are beginning to delineate the reciprocal influence of obesity and inflammation. Reviews in this series examine the activation of the innate and adaptive immune system in obesity; inflammation within diabetic islets, brain, liver, gut, and muscle; the role of inflammation in fibrosis and angiogenesis; the factors that contribute to the initiation of inflammation; and therapeutic approaches to modulate inflammation in the context of obesity and metabolic syndrome.
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“Chronic low-grade inflammation is a hallmark feature of obesity, dyslipidaemia, insulin resistance and type 2 diabetes, which are key features of the MetS (Fabbri & Rabe, 2007; Saltiel & Olefsky, 2017) .”
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Chlorogenic Acid-Induced Gut Microbiota Improves Metabolic Endotoxemia
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Vitamin B6 and Diabetes: Relationship and Molecular Mechanisms
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“Elevation of circulating fasting glucose levels, triglycerides, saturated fatty acids, inflammatory cytokines, and advanced glycation end products (AGEs), causes β-cell dysfunction and insulin resistance [9,18,21], both of which are major causes of T2DM [54,59,60].”
Background
Metadata
- Authors
- Saltiel, A. R., & Olefsky, J. M.
- Affiliations
- University of California San Diego (US)
- Venue
- Journal of Clinical Investigation
- Published
- 2017-01-03
- Volume
- 127
- Issue
- 1
- Pages
- 1-4
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- PMC
- PMC5199709
- OpenAlex
- W2567264284
- Cited by
- 2,212
- References
- 44
- Citations by year
- 2026: 261 · 2025: 318 · 2024: 265 · 2023: 255 · 2022: 308 · 2021: 280 · 2020: 270 · 2019: 136 · 2018: 80 · 2017: 36
- FWCI
- 18.93
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- University of California, San Diego (P30DK063491, DK063491)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK063491, P30DK063491)
- 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, metabolic syndrome, low-grade inflammation, insulin resistance, type 2 diabetes, adipose tissue expansion, innate immune system, adaptive immunity, neuroinflammation, liver inflammation, intestinal inflammation, skeletal muscle inflammation, fibrosis, angiogenesis, anti-inflammatory therapy
- MeSH terms
- Animals, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Humans, Inflammation, Neoplasms, Obesity, Organ Specificity, Neurodegenerative Diseases, Metabolic Syndrome
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