Low-Grade Inflammation and Oxidative Stress as Drivers of Obesity-Related Complications: A Narrative Review

Abstract

Background: The global prevalence of obesity continues to rise, with incidence rates differing markedly between regions. This narrative review synthesizes current evidence on how adipocyte dysfunction connects inflammatory and oxidative pathways to obesity-related complications, particularly cardiometabolic diseases. Methods: A narrative search of PubMed and Google Scholar was conducted to identify recent publications on the roles of inflammation and oxidative stress in obesity, providing context for the evidence discussed in this review. Results: The literature reveals that, in obesity, inflammation and oxidative stress are closely related processes originating from adipocyte dysfunction. This dysfunction increases proinflammatory cytokine secretion and triggers inflammatory immune responses. As a result, immune cells in adipose tissue—especially macrophages, but also T cells and neutrophils—adopt proinflammatory phenotypes, contributing to cytokine production and tissue remodeling. Together, impaired immune responses, chronic low-grade inflammation, and oxidative stress disrupt insulin signaling and contribute to metabolic dysfunction. Conclusion: Adipocyte dysfunction in obesity triggers immune and oxidative stress responses, driving cardiometabolic complications such as insulin resistance, type 2 diabetes, and cardiovascular diseases. Understanding these mechanisms is essential for the development of targeted therapy.