Saturated fatty acids produce an inflammatory response predominantly through the activation of TLR4 signaling in hypothalamus: implications for the pathogenesis of obesity
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In animal models of diet-induced obesity, the activation of an inflammatory response in the hypothalamus produces molecular and functional resistance to the anorexigenic hormones insulin and leptin. The primary events triggered by dietary fats that ultimately lead to hypothalamic cytokine expression and inflammatory signaling are unknown. Here, we test the hypothesis that dietary fats act through the activation of toll-like receptors 2/4 and endoplasmic reticulum stress to induce cytokine expression in the hypothalamus of rodents. According to our results, long-chain saturated fatty acids activate predominantly toll-like receptor 4 signaling, which determines not only the induction of local cytokine expression but also promotes endoplasmic reticulum stress. Rats fed on a monounsaturated fat-rich diet do not develop hypothalamic leptin resistance, whereas toll-like receptor 4 loss-of-function mutation and immunopharmacological inhibition of toll-like receptor 4 protects mice from diet-induced obesity. Thus, toll-like receptor 4 acts as a predominant molecular target for saturated fatty acids in the hypothalamus, triggering the intracellular signaling network that induces an inflammatory response, and determines the resistance to anorexigenic signals.
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Substitution of unsaturated fat for saturated fat in these protocols, or ablation of toll-like receptor signaling, reduces metabolic dysfunction and adiposity in rodents.
“Substitution of unsaturated fat for saturated fat in these protocols, or ablation of toll-like receptor signaling, reduces metabolic dysfunction and adiposity (137–143).”
From The carbohydrate-insulin model: A physiological perspective on the obesity pandemic (2021) · cites this paper as [137]
In rodents, high saturated fat content causes hyperinsulinemia, liver and muscle insulin resistance, and hypothalamic inflammation.
“which in rodents causes hyperinsulinemia, liver and muscle insulin resistance, and hypothalamic inflammation (137–143).”
From The carbohydrate-insulin model: A physiological perspective on the obesity pandemic (2021) · cites this paper as [137]
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Endurance exercise prevents metabolic distress-induced senescence in the hippocampus
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- Authors
- Milanski, M., Degasperi, G., Coope, A., Morari, J., Denis, R., Cintra, D. E., Tsukumo, D. M. L., Anhe, G., Amaral, M. E., Takahashi, H. K., Curi, R., Oliveira, H. C., Carvalheira, J. B. C., Bordin, S., Saad, M. J., & Velloso, L. A.
- Affiliations
- Universidade Estadual de Campinas (UNICAMP) (BR)
- Universidade de São Paulo (BR)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2009-01-14
- Volume
- 29
- Issue
- 2
- Pages
- 359-370
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6664935
- OpenAlex
- W2067875627
- Cited by
- 1,125
- References
- 43
- Citations by year
- 2026: 33 · 2025: 57 · 2024: 53 · 2023: 63 · 2022: 71 · 2021: 90 · 2020: 78 · 2019: 95 · 2018: 83 · 2017: 85 · 2016: 82 · 2015: 66 · 2014: 64 · 2013: 63 · 2012: 54
- FWCI
- 21.24
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Scientific Electronic Library Online (São Paulo Research Foundation, Latin American and Caribbean Center on Health Sciences Information, Conselho Nacional de Desenvolvimento Científico e Tecnológico) (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- saturated fatty acids, diet-induced obesity, hypothalamus, TLR4, TLR2, endoplasmic reticulum stress, hypothalamic inflammation, leptin resistance, insulin resistance, cytokine expression, monounsaturated fatty acids, anorexigenic hormones, dietary fat
- MeSH terms
- Animals, Antibodies, Body Weight, Disease Models, Animal, Fatty Acids, Gene Expression Regulation, Hypothalamus, Indoles, Male, Mice, Inbred C3H, Mice, Mutant Strains, Mutation, Obesity, RNA, Messenger, Signal Transduction, Cytokines, Rats, Wistar, Microglia, Immunoprecipitation, Toll-Like Receptor 2, Toll-Like Receptor 4, Mice, Rats
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.
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