Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis
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Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibrosis. Continuous low-dose infusion of the Toll-like receptor 4 ligand, lipopolysaccharide, promotes adipose tissue fibrosis. Ex vivo, lipopolysaccharide-mediated induction of fibrosis is prevented by antibodies against the profibrotic factor TGFβ1. Together, these results indicate that obesity and endotoxemia favor the development of adipose tissue fibrosis, a condition associated with insulin resistance, through immune cell Toll-like receptor 4.
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Most human studies have reported fibrosis in obese adipose tissue.
“The majority of human studies have reported fibrosis in obese AT (119-121).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [121]
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- Please cite this article in press as: Vila et al., Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity-and Endotoxemia-Associated Adipose Tissue Fibrosis, Cell Reports (2014), http://dx.doi.org/10.1016/j.celrep.2014.03.062
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- Authors
- Vila, I. K., Badin, P.-M., Marques, M.-A., Monbrun, L., Lefort, C., Mir, L., Louche, K., Bourlier, V., Roussel, B., Gui, P., Grober, J., Štich, V., Rossmeislová, L., Zakaroff-Girard, A., Bouloumié, A., Viguerie, N., Moro, C., Tavernier, G., & Langin, D.
- Affiliations
- Université Toulouse III - Paul Sabatier (FR)
- Inserm (FR)
- Charles University (CZ)
- Corresponding author
- Langin, Dominique
- ORCID
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2014-05
- Volume
- 7
- Issue
- 4
- Pages
- 1116-1129
- ISSN
- 2211-1247 (ISSN-L)
- OpenAlex
- W2102275548
- Cited by
- 165
- References
- 43
- Citations by year
- 2026: 6 · 2025: 11 · 2024: 16 · 2023: 13 · 2022: 22 · 2021: 22 · 2020: 15 · 2019: 10 · 2018: 15 · 2017: 13 · 2016: 11 · 2015: 11
- FWCI
- 8.82
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Agence Nationale de la Recherche (ANR-11-LABX-0021)
- Institut National de la Santé et de la Recherche Médicale
- 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 fibrosis, TLR4, obesity, endotoxemia, insulin resistance, macrophages, lipopolysaccharide, TGF-β1, adipocyte hypertrophy, ectopic fat deposition, high-fat diet, macrophage depletion
- MeSH terms
- Adipose Tissue, Animals, Disease Models, Animal, Fibrosis, Humans, Inflammation, Insulin Resistance, Lipopolysaccharides, Mice, Inbred C3H, Obesity, Signal Transduction, Adipocytes, Endotoxemia, Toll-Like Receptor 4, Mice, Diet, High-Fat
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