The Role of Oxidative Stress and Mitochondrial Dysfunction in Obesity-Induced Diabetes and Carcinogenesis

Obesity has emerged as a global health crisis, intricately linked to the pathogenesis of type 2 diabetes mellitus (T2DM) and various malignancies. Central to this pathological nexus is the interplay between oxidative stress and mitochondrial dysfunction. Adipose tissue expansion in obesity induces chronic inflammation, leading to the overproduction of reactive oxygen species (ROS) and impairment of mitochondrial function. This redox imbalance disrupts insulin signaling, impairs glucose homeostasis, and fosters a metabolic environment conducive to DNA damage, mutagenesis, and cancer development. Moreover, mitochondrial dysfunction exacerbates adipocyte insulin resistance and contributes to the metabolic reprogramming characteristic of cancer cells. This review critically examines the molecular and biochemical mechanisms by which oxidative stress and mitochondrial dysfunction bridge obesity to both diabetes and carcinogenesis. We explore the roles of key mediators such as NADPH oxidase, mitochondrial respiratory chain complexes, and redox-sensitive transcription factors, including NF-κB and HIF-1α. Understanding these interconnected pathways opens avenues for novel therapeutic strategies targeting redox homeostasis and mitochondrial health to mitigate obesity-driven metabolic diseases and cancer progression. Keywords: Oxidative stress, Mitochondrial dysfunction, Obesity, Type 2 diabetes mellitus, Carcinogenesis