ArticleFrontiers in immunology2023
Eicosapentaenoic acid-rich oil supplementation activates PPAR-γ and delays skin wound healing in type 1 diabetic mice.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- The effect of curcumin and high-content eicosapentaenoic acid supplementations in type 2 diabetes mellitus patients: a double-blinded randomized clinical trial.Nutrition & diabetes · 2024Trial
- Gut dysbiosis and vitamin-dependent immune regulation in degenerative musculoskeletal and bone diseases.Frontiers in immunology · 2026Review
- Immune cells in diabetic wound repair: the key to better wound management.Frontiers of medicine · 2025Review
- Supplementation with GPR120 (Ffar4) ligand omega-3 does not improve survival in murine sepsis models.American journal of physiology. Endocrinology and metabolism · 2025Article
- Acellular fish skin grafts in the treatment of diabetic wounds: Advantages and clinical translation.Journal of diabetes · 2024Review
- Krill oil: nutraceutical potential in skin health and disease.Frontiers in nutrition · 2024Review
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Delayed wound healing is a devastating complication of diabetes and supplementation with fish oil, a source of anti-inflammatory omega-3 (ω-3) fatty acids including eicosapentaenoic acid (EPA), seems an appealing treatment strategy. However, some studies have shown that ω-3 fatty acids may have a deleterious effect on skin repair and the effects of oral administration of EPA on wound healing in diabetes are unclear. We used streptozotocin-induced diabetes as a mouse model to investigate the effects of oral administration of an EPA-rich oil on wound closure and quality of new tissue formed. Gas chromatography analysis of serum and skin showed that EPA-rich oil increased the incorporation of ω-3 and decreased ω-6 fatty acids, resulting in reduction of the ω-6/ω-3 ratio. On the tenth day after wounding, EPA increased production of IL-10 by neutrophils in the wound, reduced collagen deposition, and ultimately delayed wound closure and impaired quality of the healed tissue. This effect was PPAR-γ-dependent. EPA and IL-10 reduced collagen production by fibroblasts
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