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<p>Type 2 diabetes (T2D) has been a serious health concern as its effects about 6.2% of world population. Glutathione (GSH) is a tripeptide act as natural antioxidant directly or indirectly by interacting with oxygen and nitrogen species. It is likely that oxidative stress (OS) plays a role in the development and course of T2D. Emerging research suggests that GSH, the primary cytosolic water-soluble chemical antioxidant, may help to improve T2D outcomes. It has been demonstrated that oxidative stress-mediated GSH depletion is crucial in controlling transient outward K+ currents in rat ventricular myocytes, which may be the cause of diabetes-related decreased contractility and aberrant electrical characteristics. Aldose reductase (AR) and glutathione reductase (GR) compete for the cofactor NADPH, which results in a decrease in GSH levels, as well as increased OS. Antioxidants like GSH can prevent the harm that glucose and reactive oxygen species cause to β-cells. Deletion of GSH is a significant factor underpinning heightened OS in T2DM. Supplementing diets with extra cysteine and glycine may be a secure, affordable, and creative way to boost GSH production and concentrations which can neutralise the ROS produced during anaerobic glycolysis, Schiff reaction, glycation, glucose autoxidation, and metabolism of hexosamine under supraphysiological glucose concentrations. This review is focused on the crucial antioxidant role that GSH played in management of OS and its related metabolic disease like T2DM.</p> Graphical Abstract <p></p>

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Glutathione at the Crossroads of Redox Homeostasis and Glucose Metabolism in Diabetes Mellitus

  • 期刊论文

  • 发表日期：

    2026年3月10日

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  • Shahnaz Alom,
  • Farak Ali,
  • Freddy Teilang Nongkhlaw,
  • Yangchen Doma Bhutia,
  • Bibhuti Bhusan Kakoti

摘要

Type 2 diabetes (T2D) has been a serious health concern as its effects about 6.2% of world population. Glutathione (GSH) is a tripeptide act as natural antioxidant directly or indirectly by interacting with oxygen and nitrogen species. It is likely that oxidative stress (OS) plays a role in the development and course of T2D. Emerging research suggests that GSH, the primary cytosolic water-soluble chemical antioxidant, may help to improve T2D outcomes. It has been demonstrated that oxidative stress-mediated GSH depletion is crucial in controlling transient outward K+ currents in rat ventricular myocytes, which may be the cause of diabetes-related decreased contractility and aberrant electrical characteristics. Aldose reductase (AR) and glutathione reductase (GR) compete for the cofactor NADPH, which results in a decrease in GSH levels, as well as increased OS. Antioxidants like GSH can prevent the harm that glucose and reactive oxygen species cause to β-cells. Deletion of GSH is a significant factor underpinning heightened OS in T2DM. Supplementing diets with extra cysteine and glycine may be a secure, affordable, and creative way to boost GSH production and concentrations which can neutralise the ROS produced during anaerobic glycolysis, Schiff reaction, glycation, glucose autoxidation, and metabolism of hexosamine under supraphysiological glucose concentrations. This review is focused on the crucial antioxidant role that GSH played in management of OS and its related metabolic disease like T2DM.

Graphical Abstract