Obesity is characterized by chronic low-grade inflammation that disrupts metabolic homeostasis and increases cardiometabolic risk. The postprandial period, during which individuals spend much of the day, is a critical window when nutrient absorption, lipid metabolism, and immune activation intersect. In obesity, dysfunctional adipose tissue and impaired gut barrier integrity amplify postprandial inflammatory responses through increased translocation of lipopolysaccharides and altered adipokine secretion. These processes converge on signaling pathways such as Toll-like receptor 4/nuclear factor-κB, c-Jun n-terminal kinase, and the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome, leading to insulin resistance, endothelial dysfunction, and atherogenesis. This review synthesizes evidence on the interplay between gut-derived endotoxemia and adipose tissue dysfunction in postprandial inflammation. We further highlight the modulatory roles of dietary fat quality, plant-based dietary patterns, polyphenols, omega-3 fatty acids, dietary fiber, and nuclear receptor activation, particularly through peroxisome proliferator-activated receptors (PPARs). Emerging evidence indicates that nutritional and pharmacological strategies targeting these mechanisms can attenuate postprandial inflammation and improve metabolic outcomes. A combined approach integrating personalized nutrition, functional foods, and therapies targeting PPAR isoforms may represent a promising avenue for mitigating obesity-associated postprandial inflammation and long-term cardiometabolic complications.

Cardiovascular-kidney-metabolic (CKM) syndrome integrates excess adiposity, metabolic dysfunction, kidney impairment, subclinical cardiovascular diseases, and clinical events along a staged continuum that invites unified prevention and treatment. Ultra-processed foods (UPFs) are a complex, high-prevalence exposure that may influence risk across CKM stages through nutrient profiles, additives, processing-induced compounds, and packaging-related contaminants. This review synthesizes epidemiologic, mechanistic, and translational evidence with attention to exposure definition and analytic rigor. We summarize NOVA-based UPF operationalization across dietary assessment tools, highlighting misclassification of mixed dishes, brand heterogeneity, and energy under-reporting, and we propose further examination of energy-adjusted models, calibration, and harmonized metrics. Observational studies consistently associate higher UPF intake with adiposity, diabetes, chronic kidney disease, cardiovascular events, and mortality, with modest to moderate effect sizes that are heterogeneous across populations. Mechanistic data from metabolomics, lipidomics, proteomics, and the gut microbiome converge on pathways of inflammation, lipid metabolism, oxidative and metabolic stress, and intestinal barrier dysfunction; in selected cohorts, multi-omics modules account for a substantial minority of UPF-outcome associations. We outline quality-control pipelines, batch-effect prevention/correction, and multiple-testing control necessary for reproducible diet-omics. Translationally, targeted lipidomic and proteomic panels show promise for CKM risk stratification and monitoring but require validation, clinical thresholds, and guideline endorsement. Equity and global context, including differences in product mix, food systems, and care capacity, modify population impact. We conclude with a research agenda prioritizing harmonized exposure metrics, error-aware modeling, standardized multi-omics workflows, and adequately powered, stage-specific interventions capable of testing mediation and prognostic utility.