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Purpose Metaflammation is a chronic, low-grade inflammatory state triggered by metabolic dysfunctions generally associated with unhealthy dietary habits and obesity. The consequences of metaflammation encompass various complications and comorbidities, such as adipose tissue dysfunction, insulin resistance, and impaired organ function. Thus, this narrative review aimed to synthesize current scientific evidence on obesity and diet as major triggers of metaflammation, focusing on the cellular and molecular mechanisms underlying this process, its impact on tissue and organ function, and the pathophysiological effects on major metabolic organs. Methods A search was conducted in PubMed and Google Scholar, with no publication date restrictions. Results The literature indicates that both obesity and prolonged exposure to obesogenic diets serve as central triggers for metaflammation, linking nutritional excess and metabolic dysfunction to the development of chronic diseases. Although obesity is a significant factor, maintaining an inadequate dietary pattern is sufficient to induce this inflammatory response. Given its systemic nature, this process affects the entire organism, with the kidneys, liver, and heart being particularly susceptible to its damaging effects. Conclusion Recognizing metaflammation as a crucial process defines obesity as a systemic inflammatory disease, explaining its links to various comorbidities. Thus, an integrated understanding of the immune-adipocyte and organ axes is essential for identifying new therapeutic targets and early intervention strategies.
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Vieira et al. (2026) studied this question.
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