Omega-3 supplementation: Impact on low chronic inflammation associated with obesity

Background: Supplementation of Omega-3 polyunsaturated fatty acids (PUFA), mainly alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), has been associated with beneficial effects on inflammatory processes resulting from overweight or obesity. Omega-3-PUFA commonly obtained through fish, seeds, or nuts, reduces or modulates the expression of inflammatory mediators. Despite their benefits, fish- derived products are poorly accepted, leading to omega-3 consumption deficiency. Scope and approach: This work aimed to evaluate the effects associated with omega-3-PUFA supplementation in models of overweight and/or obesity, focusing on the change in inflammation-related markers. Three groups were analyzed: ex vivo and in vivo models, and clinical trials. Inflammatory and metabolic markers, as well as transcriptomic activity modulated by omega-3, were detailed based on the source, frequency, and dosage. Likewise, different strategies for the incorporation of omega-3 in the design of new food to increase its consumption were analyzed. Key findings and conclusions: Omega-3-PUFA supplementation is strongly correlated to a decrease in inflammatory markers in blood and adipose tissue, including interleukin 18 (IL-18), interleukin 6 (IL-6), tumor necrosis factor alpha, (TNF-alpha), intracellular adhesion molecule 1 (ICAM-1), monocyte chemoattractant protein 1 (MCP1), c-reactive protein (CRP), and CX3CL1. Omega-3 can regulate the NLRP3 inflammasome activation in adipocytes and promote anti-inflammatory adipokine production. Blood triglycerides and cholesterol levels in patients affected by overweight or associated comorbidities were reduced after omega-3 supplementation. Omega-3 supplementation has demonstrated promising results in modulating low-grade chronic inflammation associated with overweight or obesity. Continuous strategies to enrich products with omega-3 are necessary to promote an increased omega-3 intake.