Summary

Oxidative stress arises when the generation of reactive oxygen species outpaces the body’s antioxidant defences, leading to damage of lipids, proteins and DNA. In disorders such as obesity, type 2 diabetes and metabolic syndrome, excessive nutrient intake and adipocyte dysfunction drive chronic redox imbalance. Mitochondrial impairment further increases production of reactive species and disrupts energy metabolism. Adipose tissue, now recognised as an active endocrine organ, secretes adipokines that influence glucose and lipid homeostasis but also modulate redox status. Such interactions underpin inflammation, insulin resistance, endothelial dysfunction and progression of organ injury. Global research efforts are focusing on identifying reliable biomarkers of oxidative damage, elucidating organ-specific pathways and evaluating interventions—from dietary modifications and exercise to pharmacological and natural antioxidant compounds—that can restore redox equilibrium and mitigate the burden of metabolic disease.

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Oxidative Stress and Metabolic Disorders publication trend

The graph below shows the total number of articles in oxidative stress and metabolic disorders across all publications each year (not limited to Nature Index journals).

Technical terms

Oxidative stress: A state in which oxidant production exceeds antioxidant capacity, causing cellular and molecular damage.

Reactive oxygen species (ROS): Oxygen-derived free radicals and peroxides that can react with cellular components to induce oxidative damage.

Metabolic syndrome: A constellation of conditions—including central obesity, hypertension, dyslipidaemia and impaired glucose tolerance—that elevate the risk of cardiovascular disease and diabetes.

Mitochondrial dysfunction: Impaired mitochondrial activity leading to reduced ATP production and increased ROS generation.

Adipokines: Signalling proteins secreted by adipose tissue that regulate metabolic and inflammatory processes.

Lipid peroxidation: Oxidative degradation of lipids that compromises membrane integrity and produces reactive aldehyde by-products.

References

  1. Nutritional load in post-prandial oxidative stress and the pathogeneses of diabetes mellitus. npj Science of Food (2024).
  2. Potential Role of Oxidative Stress in the Production of Volatile Organic Compounds in Obesity. Antioxidants (2023).
  3. Mechanisms of Oxidative Stress in Metabolic Syndrome. International Journal of Molecular Sciences (2023).

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