Mecanismo anti-inflamatório exercido pelos ácidos graxos ÔMEGA-3 em células mononucleares de indivíduos com excesso de peso: ensaio clínico randomizado

Abstract

Introduction: Omega-3 fatty acids (ω3) may modulate obesity-associated inflammation via GPR120, a G protein-coupled receptor, however, such mechanism has not been elucidated in humans. Objective: To evaluate the potential anti- inflammatory mechanism in Peripheral Blood Mononuclear Cells (PBMCs) in overweight individuals. Methods: A randomized, triple-blind, clinical trial was conducted in overweight, abdominal adiposity and nonalcoholic fatty liver disease subjects, over 19 years old, of both genders. These individuals were randomized into a group supplemented with 2.2 g of ω3 and a placebo group (mineral oil) for four weeks. In PBMCs the gene expression of Ffar4, interleukin (IL) 6 and tumor necrosis factor alpha (Tnfα) was evaluated by a real-time polymerase chain reaction, and the protein content of pro-IL18, pro-IL1β, TNFα, JNK, IL6 and IL10 was assessed by Western Blot. In the acute assay, after three hours of ω3 ingestion, the connection between GPR120/βArr2 was evaluated by immunoprecipitation. Results: A total of 39 subjects participated in the experiment, distributed as follows: 19 in the placebo group and 20 in the ω3 group. The groups were homogeneous in relation to anthropometric and body composition variables, food intake, level of physical activity, biochemical markers and plasma fatty acids.There was a significant increase, with a large effect size, for total ω3 (p<0.001; η²= 0.32) and DHA (p<0.001; η²=0.23) and a moderate effect size for EPA (p<0.001; η²=0.10), indicating treatment compliance over the four weeks.There was a reduction in TNFα protein content after four weeks of ω3 supplementation (p=0.012). In the assay of receptor connection with intracellular effector protein in human immune cells, there was such a connection after three hours of ω3 supplementation (p=0.04). Conclusion: Supplementation of ω3, in overweight individuals, as it led to reduced TNFα protein content and induced GPR120 receptor activation, demonstrated for the first time in humans.