Gut Microbiota Dysbiosis, Oxidative Stress, Inflammation, and Epigenetic Alterations in Metabolic Diseases

Summary

This narrative review synthesises evidence linking gut dysbiosis to metabolic disease development through interconnected pathways of oxidative stress, intestinal barrier dysfunction, and epigenetic alterations. The authors highlight that dysbiosis-derived metabolites such as short-chain fatty acids, lactate, and vitamins can beneficially modulate immune function and oxidative stress via epigenetic mechanisms, and discuss therapeutic interventions including dietary modification, pre- and probiotics, postbiotics, and faecal microbiota transplantation. The review emphasises that dysbiosis-associated metabolic disease phenotypes may be heritable through epigenetic mechanisms, with implications for intergenerational metabolic health.

Regional applicability

This mechanistic review is applicable globally, including to United Kingdom clinical and public health contexts, where metabolic syndrome prevalence remains high. The findings support the growing rationale for personalised nutrition and microbiota-targeted interventions in metabolic disease prevention and management in UK primary care and population health strategies.

Key measures

Gut microbiota composition and function; reactive oxygen species (ROS) production; inflammatory markers; epigenetic modifications (histone modifications, DNA methylation, RNA interference); metabolic disease parameters (obesity, insulin resistance, dyslipidemia, hypertension)

Outcomes reported

The review examines how gut microbiota dysbiosis triggers oxidative stress, inflammation, and epigenetic alterations in metabolic diseases, and evaluates dietary, prebiotic, probiotic, postbiotic, and faecal microbiota transplantation interventions to reduce these pathological processes.

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