14 August 2024 | Hamid Mostafavi Abdolmaleky, Jin-Rong Zhou
Gut microbiota dysbiosis, oxidative stress, inflammation, and epigenetic alterations are key factors in the development of metabolic diseases. Gut dysbiosis can lead to increased production of reactive oxygen species (ROS), which causes inflammation, DNA damage, immune activation, and epigenetic changes in genes involved in metabolic pathways. This can disrupt the gut barrier, allowing harmful substances to enter the bloodstream, further exacerbating oxidative stress and inflammation. However, certain gut-derived metabolites, such as short-chain fatty acids (SCFAs), can modulate oxidative stress and the immune system through epigenetic mechanisms, improving metabolic function. Metabolic diseases, including obesity, insulin resistance, and hypertension, can be transferred to the next generation via epigenetic mechanisms. This review discusses the role of gut dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, focusing on epigenetic alterations such as histone modifications, DNA methylation, and RNA interference. Potential therapeutic interventions, including dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, are explored as strategies to reduce oxidative stress, inflammation, and epigenetic alterations associated with metabolic syndrome. The review highlights the importance of gut microbiota in metabolic health and the potential of epigenetic interventions to prevent or improve metabolic diseases.Gut microbiota dysbiosis, oxidative stress, inflammation, and epigenetic alterations are key factors in the development of metabolic diseases. Gut dysbiosis can lead to increased production of reactive oxygen species (ROS), which causes inflammation, DNA damage, immune activation, and epigenetic changes in genes involved in metabolic pathways. This can disrupt the gut barrier, allowing harmful substances to enter the bloodstream, further exacerbating oxidative stress and inflammation. However, certain gut-derived metabolites, such as short-chain fatty acids (SCFAs), can modulate oxidative stress and the immune system through epigenetic mechanisms, improving metabolic function. Metabolic diseases, including obesity, insulin resistance, and hypertension, can be transferred to the next generation via epigenetic mechanisms. This review discusses the role of gut dysbiosis, oxidative stress, and inflammation in the pathogenesis of metabolic diseases, focusing on epigenetic alterations such as histone modifications, DNA methylation, and RNA interference. Potential therapeutic interventions, including dietary modifications, prebiotics, probiotics, postbiotics, and fecal microbiota transplantation, are explored as strategies to reduce oxidative stress, inflammation, and epigenetic alterations associated with metabolic syndrome. The review highlights the importance of gut microbiota in metabolic health and the potential of epigenetic interventions to prevent or improve metabolic diseases.