Eicosapentaenoic acid-rich oil supplementation activates PPAR-γ and delays skin wound healing in type 1 diabetic mice

Author:

Burger Beatriz,Sagiorato Roberta Nicolli,Silva Jéssica Rondoni,Candreva Thamiris,Pacheco Mariana R.,White Daniel,Castelucci Bianca G.,Pral Laís P.,Fisk Helena L.,Rabelo Izadora L. A.,Elias-Oliveira Jefferson,Osório Wislei Riuper,Consonni Silvio Roberto,Farias Alessandro dos Santos,Vinolo Marco Aurélio Ramirez,Lameu Claudiana,Carlos Daniela,Fielding Barbara A.,Whyte Martin Brunel,Martinez Fernando O.,Calder Philip C.,Rodrigues Hosana Gomes

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 in vitro. In vivo, topical PPAR-γ-blockade reversed the deleterious effects of EPA on wound closure and on collagen organization in diabetic mice. We also observed a reduction in IL-10 production by neutrophils in diabetic mice treated topically with the PPAR-γ blocker. These results show that oral supplementation with EPA-rich oil impairs skin wound healing in diabetes, acting on inflammatory and non-inflammatory cells.

Funder

Fundação de Amparo à Pesquisa do Estado de São Paulo

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

Publisher

Frontiers Media SA

Subject

Immunology,Immunology and Allergy

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