Introduction: Obesity is characterized by low-grade chronic inflammation, which can be modulated by lipid mediators derived from omega-3 (n-3) polyunsaturated fatty acids (PUFA). Obesity is a multifactorial disease, where genetic and environmental factors strongly interact to increase its development. In this context, the FADS1 gene encodes the delta-5 desaturase protein, which catalyzes the desaturation of PUFA. The rs174547 genetic variant of FADS1 has been associated with alterations in lipid metabolism, particularly with decreases in eicosapentaenoic acid (EPA) and arachidonic acid (AA) concentrations. Objective: To analyze the effect of an n-3-supplemented diet on the fatty acid profile and composition in red blood cells (RBCs) of obese subjects carrying the rs174547 variant of the FADS1 gene. Methodology: Seventy-six subjects with obesity were divided into two groups: omega-3 (1.5 g of n-3/day) and placebo (1.5 g of sunflower oil/day). The dietary intervention consisted of a four-month follow-up. Anthropometric, biochemical, and dietary variables were evaluated monthly. The total fatty acid profile in RBC was determined using gas chromatography. The rs174547 variant was analyzed through allelic discrimination. Results: The n-3 index (O3I) increased at the end of the intervention in both groups. Subjects carrying the CC genotype showed significant differences (minor increase) in n-6, n-3, total PUFA, EPA, DHA, and the O3I in RBCs compared to TT genotype carriers in the n-3 group. Conclusions: The diet supplemented with EPA and DHA is ideal for providing the direct products that bypass the synthesis step affected by the FADS1 rs174547 variant in subjects carrying the CC genotype. The O3I confirmed an increase in n-3 fatty acids in RBCs at the end of the intervention.

Background: Obesity increases reactive oxygen species production and alters adipokines levels, resulting in a low-grade chronic inflammation state, which contributes to tissue metabolic dysfunction. 10-gingerol, a phenol present in ginger, has shown potential anti-obesogenic effects in vitro. However, the antioxidant and anti-inflammatory properties of 10-gingerol have not been approached. The aim of this study was to investigate the effects of 10-gingerol on antioxidant enzymes’ expression and adipokine production in 3T3-L1 adipocytes in response to lipopolysaccharide (LPS)-induced inflammation. Methods: 10-gingerol antioxidant capacity was assessed through Oxygen Radical Absorbance Capacity (ORAC) , Ferric Reducing Antioxidant Power (FRAP), and radical scavenging activity of 2,2-diphenyl-2-picrylhydrazyl (DPPH) assays. 3T3-L1 cells were differentiated and stimulated with 100 ng/mL LPSs. Then, 15 µg/mL 10-gingerol was added for 48 h. The mRNA expression and protein abundance of antioxidant enzymes were evaluated by qPCR and Western blot, respectively. Adipokine levels were determined by ELISA. Results: 10-gingerol showed low FRAP and DPPH values but a moderate ORAC value. Moreover, 10-gingerol increased Gpx1 and Sod1 but downregulated Cat expression. Additionally, 10-gingerol significantly increased CAT and GPx1 levels but not SOD-1. Finally, adiponectin and leptin concentrations were increased while resistin and tumor necrosis factor alpha (TNFα) were decreased by 10-gingerol. Conclusions: 10-gingerol presented antioxidant potential by increasing antioxidant enzymes and attenuated LPS-induced inflammation by modulating adipokines in 3T3-L1 adipocytes.

Background/Objectives: Obesity is associated with chronic low-grade inflammation. Polyunsaturated fatty acids (PUFAs) such as omega-3 (n-3), are essential in anti-inflammatory processes. Therefore, the aim of this study was to evaluate the effect of a dietary intervention along with supplementation of 1.8 g of marine n-3 PUFAs on anthropometric, biochemical, and inflammatory markers in adults. Methods: An 8-week double-blind randomized clinical trial was conducted with a diet (200 kcal/day reduction each 4 weeks based on the estimated basal caloric expenditure) containing a n-6/n-3 PUFA ratio ≤ 5:1, along with daily 1.8 g of marine n-3 supplementation (EPA and DHA) vs. active placebo 1.6 g (ALA). A total of 40 subjects were included in the study, 21 in the marine omega-3 group and 19 in the active placebo group. Inclusion criteria included subjects aged 25 to 50 years with obesity as determined by body mass index (BMI) and/or abdominal obesity according to ATP III criteria. Results: The marine omega-3 supplemented group had a better effect compared to the active placebo group, increasing Resolvin D1 [129.3 (−90.1–193.5) vs. −16.8 (−237.8–92.5) pg/mL, p = 0.041], IL-10 [1.4 (−0.7–4.6) vs. −2.0 (−5–0.05) pg/mL, p = 0.001], and decreasing IL-6 [−0.67 (2.72–−0.59) vs. 0.03 (−0.59–1.84) pg/mL, p = 0.015], and MCP-1 [−29.6 (−94.9–5.50) vs. 18.3 (−97.3–66.35) pg/mL, p = 0.040]. Conclusions: A diet supplemented with marine n-3 improves inflammatory markers by increasing systemic levels of Resolvin D1 and IL-10 and decreasing IL-6 and MCP-1.

Background: It is widely accepted that low-grade chronic inflammation in obesity worsens the metabolic state and threatens patients’ lives in a long-term manner. In fact, diet therapy is the first-line treatment in which relevant nutrients such as the omega-3 polyunsaturated fatty acids (ω-3 PUFA) must be adequately consumed to counteract the established inflammation. In particular, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been identified as agonists of cellular receptors, including the free fatty acid receptor 4 (FFAR4), which regulates anti-inflammatory pathways associated with enhanced insulin sensitivity. However, the expression and activation of this receptor in peripheral blood mononuclear cells (PBMC) remains poorly investigated in humans. Objective: This study aimed to evaluate the effect of a diet supplemented with marine ω-3 PUFA on FFAR4 receptor activation and inflammatory markers in peripheral blood mononuclear cells in subjects with obesity. Methodology: A double-blind, randomized clinical trial (NCT05068557) was conducted over two months (eight weeks) in 55 obese individuals (aged 25–59 years). Participants were randomly assigned to one of two groups: an active placebo group (1.6 g/day of alpha-linolenic acid) or a marine ω-3 group (1080 mg of EPA and 720 mg of DHA). Both groups followed a dietary regimen with progressive calorie restriction (−200 kcal/day during weeks 0–4 and −400 kcal/day during weeks 4–8) in addition to supplementation. Results: Following the intervention, both groups showed significant improvements in body composition and biochemical parameters. Supplementation with EPA and DHA enhanced FFAR4 activation at the end of the intervention. Moreover, there was a reduction in the expression of JNK and IKKβ genes, as well as in serum levels of TNF-α, IL-6, and IL-18. In contrast, IL-10 levels increased significantly both within and between the groups. Conclusions: Marine ω-3 PUFA supplementation, in the context of a dietary intervention, promotes FFAR4 activation, thereby contributing to the modulation of the inflammatory response in human PBMC.

Obesity is associated with chronic low-grade inflammation. Polyunsaturated fatty ac-ids such as omega-3 (n-3), are essential in the pro-resolution of inflammation. An 8-week double-blind randomized clinical trial was conducted with a n-6:n-3, 5:1 ratio, along with daily 1.8 g of n-3 supplementation vs. placebo. A total of 40 subjects were included, 21 in omega 3 group and 19 in placebo group. The n-3 supplementation had a superior effect compared to placebo increasing levels of Resolvin D1 [129.3 (-90.1 - 193.5) vs. -16.8 (-237.8 - 92.5) pg/mL, p=0.041], IL-10 [1.4 (-0.7 - 4.6) vs. -2.0 (-5 - 0.05) pg/mL, p=0.001], and decreasing IL-6 [-0.67 (2.72 - -0.59) vs. 0.03 (-0.59 - 1.84) pg/mL p=0.015], and MCP-1 [-29.6 (-94.9 - 5.50) vs. 18.3 (-97.3 - 66.35) pg/mL, p=0.040]. In con-clusion, n-3 supplementation promoted resolution of inflammation by increasing sys-temic levels of Resolvin D1, IL-10, and decreasing IL-6 and MCP-1.

Background: Neck circumference (NC) is a simple anthropometric index of upper-body subcutaneous adiposity. Its relationship with inflammatory cytokines, particularly the anti-inflammatory cytokine IL-10, remains poorly explored, especially in Latin-American populations. Methods: This cross-sectional study analyzed data from 80 Mexican adults with obesity (40 women and 40 men). NC, waist circumference (WC), and body mass index (BMI) were measured according to standardized ISAK and NHANES protocols. Fasting glucose, insulin, lipid profile, and HbA1c were evaluated. Finally, serum TNF-α, IL-6, IL-18, IL-10, and hs-CRP were quantified from a subsample. Correlation coefficients and sex-stratified multiple linear regression models adjusted for age and BMI were performed. Results: In the overall sample, neck circumference (NC) was positively associated with triglycerides, VLDL-C, insulin, and HbA1c, and inversely associated with HDL-C. Sex-stratified analyses revealed marked differences. In women, NC showed strong and independent associations with triglycerides, VLDL-C, IL-10, and the IL-10/TNF-α ratio, whereas these associations were not observed in men. Similarly, waist circumference was independently associated with IL-10, and BMI was associated with hs-CRP. Conclusions: NC may serve as a useful surrogate marker of upper-body adiposity and is independently associated with triglycerides, VLDL-C, IL-10, and the IL-10/TNF-α ratio exclusively in women with obesity. These exploratory findings highlight sex-specific differences in the adiposity–inflammation axis and underscore the need for larger longitudinal studies and sex-tailored approaches in obesity research.