O Intestino como Gatilho Imunológico na Disfunção Metabólica e Inflamatória da Obesidade

Obesity is a chronic and multifactorial condition associated with severe comorbidities, whose pathophysiology involves low-grade inflammation and insulin resistance. The intestinal microbiota plays a central role in this process, acting as a metabolic regulator. However, its dysregulation, usually caused by hypercaloric diets, compromises the intestinal barrier and increases permeability. A narrative systematic review was conducted according to the PRISMA guidelines, structured using the PICO model, with searches performed in PubMed/MEDLINE, Scopus, and SciELO databases (2015–2025), including relevant classical articles. Original studies in humans, published in English, Spanish, or Portuguese, were selected, while studies using animal models or presenting inconclusive data were excluded. The screening process, conducted blindly via Rayyan, was carried out in stages (titles, abstracts, and full texts). The included studies were synthesized in tables with key information and organized according to the axes TLR4, SCFAs, LPS, and intestinal permeability. The studies show that TLR4 activation, induced by LPS and saturated fatty acids, promotes systemic inflammation and metabolic dysfunction through the modulation of intestinal microbiota and barrier permeability. Dysbiosis, characterized by an increase in LPS-producing bacteria, sustains metabolic endotoxemia and chronic immune activation, with a direct impact on the liver, adipose tissue, and pancreas. Dietary interventions, weight loss, bariatric surgery, and probiotics have shown efficacy in restoring intestinal homeostasis, reducing inflammation, and modulating cardiometabolic risk.