Cited by 2,319Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismImmune cells in cancer

Inflammatory links between obesity and metabolic disease

Open access
Lumeng, Carey N., Saltiel, Alan R.·2011·Journal of Clinical Investigation

Abstract

The obesity epidemic has forced us to evaluate the role of inflammation in the health complications of obesity. This has led to a convergence of the fields of immunology and nutrient physiology and the understanding that they are inextricably linked. The reframing of obesity as an inflammatory condition has had a wide impact on our conceptualization of obesity-associated diseases. In this Review, we highlight the cellular and molecular mechanisms at play in the generation of obesity-induced inflammation. We also emphasize how defining the immune regulation in metabolic tissues has broadened the understanding of the diversity of inflammatory responses.

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Crossref · 10.1172/jci57132

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  • Higher circulating levels of these pro-inflammatory markers are reported in adolescents with type 2 diabetes.

    “Increased circulating concentrations of these pro-inflammatory markers are reported in adolescents with T2DM 30 .”

    From Type 2 diabetes in adolescents and young adults (2018) · cites this paper as [30]

    The Antiinflammatory therapies for metabolic disease section (page unavailable) reports that treatment in type 2 diabetes decreases systemic inflammatory markers, supporting a general link between these markers and the disease. The Pancreatic islets section discusses adolescents only in relation to adipose tissue, not circulating marker concentrations in adolescents with type 2 diabetes. That population-specific finding is not supported by our copy. (LLM, conf=0.77)

    Experimental — accuracy not yet measured
  • Aged WAT is characterized by a proinflammatory microenvironment with elevated expression of inflammatory genes associated with metabolic disease.

    “Aged WAT is characterized by a proinflammatory microenvironment with elevated expression of inflammatory genes associated with metabolic disease (39).”

    From Metabolic impact of endogenously produced estrogens by adipose tissue in females and males across the lifespan (2025) · cites this paper as [39]

    In “The nature of obesity-induced inflammation” (page unavailable), the paper reports overexpressed inflammatory genes in adipose tissue associated with obesity and metabolic disease. It also describes a shift toward proinflammatory macrophage signals with increasing adiposity. These passages support the inflammatory-gene and microenvironment aspects, but they concern obesity, not aged white adipose tissue; the aging qualifier is unsupported. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Perturbations in immune function exacerbate neurodegeneration and metabolic diseases.

    “Perturbations in immune function have been demonstrated to exacerbate neurodegeneration and metabolic diseases (Lumeng and Saltiel, 2011; Ransohoff, 2016; Reilly and Saltiel, 2017).”

    From Deletion of the Alzheimer’s disease risk gene Abi3 locus results in obesity and systemic metabolic disruption in mice (2022) · cites this paper as Lumeng and Saltiel, 2011

    The nature of obesity-induced inflammation (page unavailable) links inflammatory immune responses to metabolic dysfunction, and the Conclusion describes inflammation worsening insulin resistance and diabetes progression. The paper discusses brain inflammation in relation to metabolic function, but the passages do not show that immune perturbations exacerbate neurodegeneration; its mention of neuronal injury describes injury inducing inflammation instead. (LLM, conf=0.88)

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Cites

2 retracted

Flagged first, then by citations

Research works printed but not linked: 4

  1. Hotamisligil GS. Inflammation and metabolic dis- orders. Nature. 2006;444(7121):860-867.
  2. Maedler K, et al. Glucose-induced beta cell pro- duction of IL-1beta contributes to glucotoxic- ity in human pancreatic islets. J Clin Invest. 2002; 110(6):851-860.
  3. Thaler JP, Choi SJ, Schwartz MW, Wisse BE. Hypo- thalamic inflammation and energy homeosta- sis: resolving the paradox. Front Neuroendocrinol. 2010;31(1):79-84.
  4. Challis JR, Lockwood CJ, Myatt L, Norman JE, Strauss JF 3rd, Petraglia F. Inflammation and preg- nancy. Reprod Sci. 2009;16(2):206-215.

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Authors
Lumeng, C. N., & Saltiel, A. R.
Affiliations
University of Michigan (US)
Corresponding author
Lumeng, Carey N.
Venue
Journal of Clinical Investigation
Published
2011-06-01
Volume
121
Issue
6
Pages
2111-2117
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2165604976
Cited by
2,319
References
124
Citations by year
2026: 109 · 2025: 111 · 2024: 105 · 2023: 111 · 2022: 154 · 2021: 187 · 2020: 173 · 2019: 177 · 2018: 186 · 2017: 211 · 2016: 176 · 2015: 163 · 2014: 165 · 2013: 155 · 2012: 108
FWCI
16.91
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK090262, R01DK060591, K08DK078851)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Keywords
obesity, inflammation, metabolic disorders, obesity-related comorbidities, immune regulation, metabolic tissues
MeSH terms
Acute-Phase Proteins, Adipose Tissue, Animals, Anti-Inflammatory Agents, Energy Metabolism, Fibrosis, Humans, Hypothalamus, Inflammation, Leukocytes, Liver, Macrophages, Metabolic Diseases, Models, Biological, Obesity, Organ Specificity, Cytokines, Disease Progression, Muscle, Skeletal, Peroxisome Proliferator-Activated Receptors

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