Inflammatory Pathways of Metabolic Disease: From Obesity to Systemic Dysfunction

Resumen

Metabolic inflammation (metaflammation) is a key biological process linking obesity, insulin resistance, and chronic disease. This review integrates molecular and epidemiological evidence to explain how low-grade inflammation acts as both the cause and consequence of metabolic dysfunction. Adipose tissue functions as an immunometabolic organ, releasing cytokines and adipokines that disrupt insulin signaling and promote systemic complications. Major mediators—TNF-α, IL-6, CRP, leptin, resistin, and decreased adiponectin—constitute a proinflammatory network underlying metabolic syndrome, cardiovascular disease, and fatty liver. Using an integrative approach based on the DMAIC model (Define–Measure–Analyze–Improve–Control), this review synthesizes data from international and Latin American studies, emphasizing Mexico, Colombia, and Ecuador. Findings indicate that inflammation begins in adipose tissue and extends to the liver, skeletal muscle, cardiovascular system, and central nervous system, creating a self-perpetuating feedback loop. Regional data show high obesity and metabolic syndrome prevalence, driven by biological vulnerability and social factors such as diet, urbanization, and limited healthcare access. Effective management requires a multilevel strategy combining lifestyle modification, pharmacologic agents, targeted anti-inflammatory compounds, and public health interventions. Lifestyle change remains the cornerstone, supported by metabolic drugs and multidisciplinary programs. The evidence supports metaflammation as the unifying mechanism driving global metabolic disease. Recognizing it as a therapeutic and preventive target reframes clinical priorities, emphasizing the restoration of immunometabolic balance through integrative, context-specific action.