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Abstract <p>Hepatic insulin resistance is a key aspect of obesity-linked metabolic dysfunction, but the molecular mechanisms are still insufficiently understood. Now, a new study shows that reactive oxygen species (ROS) act as signaling mediators that reprogram hepatic glucose metabolism through reversible oxidative modification of phosphorylated GSK-3β. They demonstrate that ROS-dependent sulfenylation of GSK-3β at Cys178 restores its kinase activity while AKT signaling is still intact. This leads to inhibition of glycogenesis and activation of gluconeogenesis via FOXO1, thereby providing a mechanistic explanation for early hepatic insulin resistance mediated by oxidative stress.</p>

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How oxidative stress leads to hepatic insulin resistance

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月21日

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  • Mariia Khamdan,
  • Alexander Bartelt

摘要

Abstract

Hepatic insulin resistance is a key aspect of obesity-linked metabolic dysfunction, but the molecular mechanisms are still insufficiently understood. Now, a new study shows that reactive oxygen species (ROS) act as signaling mediators that reprogram hepatic glucose metabolism through reversible oxidative modification of phosphorylated GSK-3β. They demonstrate that ROS-dependent sulfenylation of GSK-3β at Cys178 restores its kinase activity while AKT signaling is still intact. This leads to inhibition of glycogenesis and activation of gluconeogenesis via FOXO1, thereby providing a mechanistic explanation for early hepatic insulin resistance mediated by oxidative stress.