The article reviews the role of gut microbiota dysbiosis, oxidative stress, inflammation, and epigenetic alterations in the development of metabolic diseases. Gut dysbiosis, characterized by an imbalance in the gut microbiome, can lead to excessive production of reactive oxygen species (ROS), disrupting gut barrier integrity and activating the immune system, thereby causing inflammation and epigenetic alterations. These changes can further enhance ROS production and inflammation, leading to metabolic disorders such as obesity, insulin resistance, dyslipidemia, and hypertension. However, specific gut-derived metabolites, like short-chain fatty acids (SCFAs), lactate, and vitamins, can modulate oxidative stress and the immune system through epigenetic mechanisms, improving metabolic function. The article also discusses the transgenerational transmission of gut microbiota-related metabolic diseases through epigenetic mechanisms and explores potential therapeutic interventions, including dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, which may reduce oxidative stress and inflammation associated with metabolic syndrome by altering gut microbiota and epigenetic alterations. The review highlights the crucial role of gut microbiota dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, emphasizing the importance of epigenetic alterations and potential interventions to prevent or improve these conditions.The article reviews the role of gut microbiota dysbiosis, oxidative stress, inflammation, and epigenetic alterations in the development of metabolic diseases. Gut dysbiosis, characterized by an imbalance in the gut microbiome, can lead to excessive production of reactive oxygen species (ROS), disrupting gut barrier integrity and activating the immune system, thereby causing inflammation and epigenetic alterations. These changes can further enhance ROS production and inflammation, leading to metabolic disorders such as obesity, insulin resistance, dyslipidemia, and hypertension. However, specific gut-derived metabolites, like short-chain fatty acids (SCFAs), lactate, and vitamins, can modulate oxidative stress and the immune system through epigenetic mechanisms, improving metabolic function. The article also discusses the transgenerational transmission of gut microbiota-related metabolic diseases through epigenetic mechanisms and explores potential therapeutic interventions, including dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, which may reduce oxidative stress and inflammation associated with metabolic syndrome by altering gut microbiota and epigenetic alterations. The review highlights the crucial role of gut microbiota dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, emphasizing the importance of epigenetic alterations and potential interventions to prevent or improve these conditions.