分子薬学および有機プロセス研究ジャーナル

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Molecular Mechanisms Linking Oxidative Stress and Diabetes Mellitus

Santella Yasunori

Diabetes mellitus is a prevalent metabolic disorder characterized by high blood glucose levels, and oxidative stress has been implicated in its pathogenesis. Oxidative stress refers to an imbalance between the production of reactive oxygen species and the body's ability to neutralize them. This review aims to provide an overview of the molecular mechanisms linking oxidative stress and diabetes mellitus.

Numerous studies have revealed that oxidative stress plays a crucial role in the development and progression of diabetes mellitus. Excessive ROS production and impaired antioxidant defense mechanisms contribute to the generation of oxidative stress. This, in turn, leads to the activation of stress-sensitive signaling pathways, such as c-Jun N-terminal kinase and nuclear factor kappa B, resulting in insulin resistance. Oxidative stress also induces pancreatic beta-cell dysfunction through mechanisms such as apoptosis, mitochondrial dysfunction, and altered gene expression. Furthermore, oxidative stress disrupts glucose homeostasis by impairing insulin signaling in insulinsensitive tissues like skeletal muscle, liver, and adipose tissue.

Understanding the molecular mechanisms connecting oxidative stress and diabetes mellitus is critical for developing effective therapeutic strategies. By targeting these pathways, it may be possible to mitigate oxidative stress and restore normal cellular function, thus improving the management and outcomes of diabetes mellitus. Further research in this area is needed to identify novel therapeutic targets and interventions for the prevention and treatment of diabetes mellitus.