ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020
Resolvin E1 derived from eicosapentaenoic acid prevents hyperinsulinemia and hyperglycemia in a host genetic manner.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 56 citations in OpenAlex.
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- Endogenous Lipid Signals in Energy Homeostasis and Fibrosis.Biomolecules · 2026Review
- Fifteen years of the Diversity Outbred mouse model: a review.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Role play of regulatory T cells and resolvins in type 2 diabetes.Frontiers in immunology · 2026Review
- Melanoregulin Deficiency Affects Bone Maintenance and Lean Body Mass.bioRxiv : the preprint server for biology · 2025Article
- Inflammation-resolution signalling in cardiac repair, remodelling, and heart failure.European heart journal open · 2025Review
- Genetic deletion of Alx/Fpr2 differentially regulates pulmonary inflammation in the absence and presence of acute lung injury.ImmunoHorizons · 2025Article
- Emerging mechanisms of organ crosstalk: The role of oxylipins.Nutrition bulletin · 2025Review
- Dietary Eicosapentaenoic Acid Improves Ozone-Induced Pulmonary Inflammation in C57BL/6 Mice.The Journal of nutrition · 2025Article
- Inflammation and resolution in obesity.Nature reviews. Endocrinology · 2025 · on this mapReview
- Oxylipins Derived from PUFAs in Cardiometabolic Diseases: Mechanism of Actions and Possible Nutritional Interactions.Nutrients · 2024Review
- Brown Adipose Tissue Activation in Humans Increases Plasma Levels of Lipid Mediators.The Journal of clinical endocrinology and metabolism · 2024Article
- Is Lipid Metabolism of Value in Cancer Research and Treatment? Part II: Role of Specialized Pro-Resolving Mediators in Inflammation, Infections, and Cancer.Metabolites · 2024Review
- Emerging mechanisms of obesity-associated immune dysfunction.Nature reviews. Endocrinology · 2024Review
- Do patients benefit from omega-3 fatty acids?Cardiovascular research · 2024Review
- Article
- Extrinsic and intrinsic modulators of inflammation-resolution signaling in heart failure.American journal of physiology. Heart and circulatory physiology · 2023Review
- Behavioral changes inFrontiers in neuroscience · 2023Article
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
Eicosapentaenoic acid (EPA) has garnered attention after the success of the REDUCE-IT trial, which contradicted previous conclusions on EPA for cardiovascular disease risk. Here we first investigated EPA's preventative role on hyperglycemia and hyperinsulinemia. EPA ethyl esters prevented obesity-induced glucose intolerance, hyperinsulinemia, and hyperglycemia in C57BL/6J mice. Supporting NHANES analyses showed that fasting glucose levels of obese adults were inversely related to EPA intake. We next investigated how EPA improved murine hyperinsulinemia and hyperglycemia. EPA overturned the obesity-driven decrement in the concentration of 18-hydroxyeicosapentaenoic acid (18-HEPE) in white adipose tissue and liver. Treatment of obese inbred mice with RvE1, the downstream immunoresolvant metabolite of 18-HEPE, but not 18-HEPE itself, reversed hyperinsulinemia and hyperglycemia through the G-protein coupled receptor ERV1/ChemR23. To translate the findings, we determined if the effects of RvE1 were dependent on host genetics. RvE1's effects on hyperinsulinemia and hyperglycemia were divergent in diversity outbred mice that model human genetic variation. Secondary SNP analyses further confirmed extensive genetic variation in human RvE1/EPA-metabolizing genes. Collectively, the data suggest EPA prevents hyperinsulinemia and hyperglycemia, in part, through RvE1's activation of ERV1/ChemR23 in a host genetic manner. The studies underscore the need for personalized administration of RvE1 based on genetic/metabolic enzyme profiles.
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