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Cited by 194Inflammasome and immune disordersAdipokines, Inflammation, and Metabolic DiseasesImmune Response and Inflammation

Free fatty acids as modulators of the NLRP3 inflammasome in obesity/type 2 diabetes

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Legrand-Poels, Sylvie, Esser, Nathalie, L’homme, Laurent, Scheen, André, Paquot, Nicolas, Piette, Jacques·2014·Biochemical Pharmacology
DOI 10.1016/j.bcp.2014.08.013
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Abstract

Free fatty acids (FFAs) are metabolic intermediates that may be obtained through the diet or synthesized endogenously. In addition to serving as an important source of energy, they produce a variety of both beneficial and detrimental effects. They play essential roles as structural components of all cell membranes and as signaling molecules regulating metabolic pathways through binding to nuclear or membrane receptors. However, under conditions of FFAs overload, they become toxic, inducing ROS production, ER stress, apoptosis and inflammation. SFAs (saturated fatty acids), unlike UFAs (unsaturated fatty acids), have recently been proposed as triggers of the NLRP3 inflammasome, a molecular platform mediating the processing of IL-1β in response to infection and stress conditions. Interestingly, UFAs, especially ω-3 FAs, inhibit NLRP3 inflammasome activation in various settings. We focus on emerging models of NLRP3 inflammasome activation with a special emphasis on the molecular mechanisms by which FFAs modulate the activation of this complex. Taking into consideration the current literature and FFA properties, we discuss the putative involvement of mitochondria and the role of cardiolipin, a mitochondrial phospholipid, proposed to be sensed by NLRP3 after release, exposure and/or oxidation. Finally, we review how this SFA-mediated NLRP3 inflammasome activation contributes to the development of both insulin resistance and deficiency associated with obesity/type 2 diabetes. In this context, we highlight the potential clinical use of ω-3 FAs as anti-inflammatory compounds.

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  • Dietary palmitic acid activates both the NLRP3 inflammasome and mTORC1.

    “and activates both the NLRP3 inflammasome and mTORC116,17”

    From Sebaceous-immunobiology is orchestrated by sebum lipids (2017) · cites this paper as [17]

    Section 4 reports that palmitate activated the NLRP3 inflammasome in LPS-primed macrophages, supporting that part of the claim in a specific cell-culture setting. The passages found do not report that palmitate activates mTORC1 or establish the claim for dietary palmitic acid. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

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Authors
Legrand-Poels, S., Esser, N., L’homme, L., Scheen, A., Paquot, N., & Piette, J.
Affiliations
  • University of Liège (BE)
  • Centre Hospitalier Universitaire de Liège (BE)
Corresponding author
Legrand-Poels, Sylvie
ORCID
Venue
Biochemical Pharmacology
Publisher
Elsevier BV
Published
2014-11
Volume
92
Issue
1
Pages
131-141
ISSN
0006-2952 (ISSN-L)
DOI
10.1016/j.bcp.2014.08.013
OpenAlex
W2007479707
Cited by
194
References
127
Citations by year
2026: 9 · 2025: 15 · 2024: 23 · 2023: 17 · 2022: 14 · 2021: 17 · 2020: 10 · 2019: 20 · 2018: 17 · 2017: 22 · 2016: 13 · 2015: 17
FWCI
1.63
Type
journal article
Language
en
Open access
Licence
Locations
  • Biochemical Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
  • ORBi (University of Liège) (submittedVersion, other-oa)
Funders
  • Fonds De La Recherche Scientifique - FNRS
  • Belgian Federal Science Policy Office (P7/32)
  • Fonds Léon Fredericq
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
free fatty acids, NLRP3 inflammasome, obesity, type 2 diabetes, saturated fatty acids, omega-3 fatty acids, unsaturated fatty acids, IL-1β processing, cardiolipin, insulin resistance, inflammation, fatty acid overload
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Carrier Proteins, Diabetes Mellitus, Type 2, Fatty Acids, Nonesterified, Gene Expression Regulation, Humans, Insulin Resistance, Obesity, Inflammasomes

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