An immune origin of type 2 diabetes?
Open accessAbstract
Subclinical, low-grade systemic inflammation has been observed in patients with type 2 diabetes and in those at increased risk of the disease. This may be more than an epiphenomenon. Alleles of genes encoding immune/inflammatory mediators are associated with the disease, and the two major environmental factors the contribute to the risk of type 2 diabetes-diet and physical activity-have a direct impact on levels of systemic immune mediators. In animal models, targeting of immune genes enhanced or suppressed the development of obesity or diabetes. Obesity is associated with the infiltration and proinflammatory activity of macrophages in adipose tissue, and immune mediators may be important regulators of insulin resistance, mitochondrial function, ectopic lipid storage and beta cell dysfunction or death. Intervention studies targeting these pathways would help to determine the contribution of an activated innate immune system to the development of type 2 diabetes.
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Macrophages accumulate in adipose tissue in obesity and may be major contributors to adipokine production.
“It is now recognised that macrophages accumulate in the adipose tissue in obesity (10,11) (Fig. 1) and that these may represent major contributors to the production of adipokines (12,13) .”
From Dietary factors and low-grade inflammation in relation to overweight and obesity (2011) · cites this paper as [11]
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- Authors
- Kolb, H., & Mandrup-Poulsen, T.
- Affiliations
- Deutsches Diabetes-Zentrum e.V. (DE)
- Karolinska Institutet (SE)
- Corresponding author
- Kolb, H.
- Venue
- Diabetologia
- Published
- 2005-04-30
- Volume
- 48
- Issue
- 6
- Pages
- 1038-1050
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2078830150
- Cited by
- 394
- References
- 226
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 11 · 2023: 12 · 2022: 15 · 2021: 11 · 2020: 11 · 2019: 16 · 2018: 18 · 2017: 9 · 2016: 20 · 2015: 18 · 2014: 31 · 2013: 20 · 2012: 25
- FWCI
- 4.01
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Bundesministerium für Gesundheit
- Novo Nordisk
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Keywords
- type 2 diabetes, low-grade inflammation, innate immunity, immune mediators, genetic susceptibility, obesity, insulin resistance, beta-cell dysfunction, mitochondrial function, diet, physical activity
- MeSH terms
- Adipose Tissue, Animals, Diabetes Mellitus, Type 2, Disease Models, Animal, Humans, Inflammation, Macrophages, Obesity
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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