Metabolic endotoxemia: a molecular link between obesity and cardiovascular risk
Open accessAbstract
Obesity is associated with significantly increased cardiovascular (CV) risk and mortality. Several molecular mechanisms underlying this association have been implied, among which the intestinal barrier has gained a growing interest. In experimental models of obesity, significant alterations in the intestinal barrier lead to increased intestinal permeability, favoring translocation of microbiome-derived lipopolysaccharide to the bloodstream. This has been shown to result in a two- to threefold increase in its serum concentrations, a threshold named ‘metabolic endotoxemia’ (ME). ME may trigger toll-like receptor 4-mediated inflammatory activation, eliciting a chronic low-grade proinflammatory and pro-oxidative stress status, which may result in high CV risk and target-organ damage. In this review, we discuss the potential molecular implications of ME on several CV risk factors, such as obesity, insulin resistance, dyslipidemia, and oxidative stress, as well as its potential impact on the development of CV target-organ disease.
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Endotoxemia may occur secondary to increased intestinal permeability resulting from extreme physiologic stress, ethanol exposure, or a Western diet high in carbohydrate and saturated fat.
“and secondary to increased intestinal permeability resulting from extreme physiologic stress,32 ethanol exposure,33 or a “fast-food style” Western diet, high in both carbohydrate and saturated fat.34”
From The Gut Microbiome and the Brain (2014) · cites this paper as [34]
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Obesity, inflammation, and the gut microbiota
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Stress induces endotoxemia and low-grade inflammation by increasing barrier permeability
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Gut microbiota influences pathological angiogenesis in obesity‐driven choroidal neovascularization
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Endotoxemia, nutrition, and cardiometabolic disorders
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- Authors
- Neves, A. L., Coelho, J., Couto, L., Leite-Moreira, A., & Roncon-Albuquerque, R.
- Affiliations
- Universidade do Porto (PT)
- Venue
- Journal of Molecular Endocrinology
- Publisher
- Bioscientifica
- Published
- 2013-08-12
- Volume
- 51
- Issue
- 2
- Pages
- R51-R64
- ISSN
- 0952-5041 (ISSN-L)
- 1479-6813
- OpenAlex
- W2074238456
- Cited by
- 211
- References
- 94
- Citations by year
- 2026: 10 · 2025: 5 · 2024: 16 · 2023: 12 · 2022: 25 · 2021: 17 · 2020: 36 · 2019: 16 · 2018: 16 · 2017: 19 · 2016: 17 · 2015: 13 · 2014: 7 · 2013: 2
- FWCI
- 1.22
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Molecular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
- Keywords
- metabolic endotoxemia, obesity, cardiovascular risk, intestinal permeability, intestinal barrier, lipopolysaccharide, gut microbiota, TLR4, low-grade inflammation, oxidative stress, insulin resistance, dyslipidemia, target organ damage
- MeSH terms
- Animals, Cardiovascular Diseases, Humans, Immunity, Innate, Intestinal Mucosa, Intestines, Obesity, Risk Factors, Endotoxemia
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.
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