Obesity is a chronic disease accompanied by a growing prevalence worldwide, influenced by both environmental and genetic factors. It is identified by the surplus deposition of fat tissue, primarily due to adipogenesis—the differentiation of stem cells into adipocytes—which leads to hyperplasia and/or hypertrophy. Mature adipocytes store triglycerides, mainly synthesized through lipogenesis. In obesity, upregulated lipogenesis can increase the generation of reactive oxygen species (ROS), leading to oxidative stress (OS) by disrupting cellular redox balance. This OS is closely associated with adipogenesis and is fundamentally involved in the progression of obesity-linked comorbidities, including insulin resistance, type 2 diabetes, cardiovascular disease, and metabolic-associated fatty liver disease. Although surgical and pharmacological approaches are available, long-term and fully effective treatments for weight management remain limited. Lifestyle changes, such as adjustments in diet and enhanced physical exercise, continue to be the primary strategies for weight control. Therefore, a detailed knowledge of the mechanisms through which ROS influence obesity may offer novel therapeutic opportunities. Accordingly, the aim of this chapter is to explore the mechanisms through which ROS participate in triggering and worsening obesity.