Targeting postprandial inflammation through personalized nutrition and PPAR activation represents a promising avenue for mitigating obesity-associated cardiometabolic complications.
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.
Shahamati et al. (Mon,) studied this question.