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<p>Insulin resistance (IR) is the key pathogenic factor of type 2 diabetes (T2DM) and its associated metabolic diseases. Mitochondrial dysfunction and inadequate mitophagy are central to this pathology. Curcumin, the main bioactive compound of <i>Curcuma longa</i>, has been reported to enhance insulin sensitivity, yet the mechanism in hepatocytes remains debated. Here we investigated whether curcumin alleviates hepatocyte IR by targeting PTEN-induced putative kinase 1 (PINK1)/ Parkin-dependent mitophagy. We induced IR in HepG2 cells with palmitic acid (PA) and then treated with curcumin. To verify the mechanism, we used PINK1 siRNA (siPINK1) and the mitophagy blocker Mdivi-1. Glucose uptake, glycogen content, lipid accumulation, phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (Akt)/ glucose transporter 4 (GLUT4) signaling, mitochondrial function, and mitophagy markers were quantified by flow cytometry, glycogen assay kit, Oil Red O staining, confocal imaging, and Western blot. Curcumin mitigated PA-induced IR, increased PI3K/Akt phosphorylation and GLUT4 expression, promoted GLUT4 translocation to the plasma membrane, restored mitochondrial membrane potential and ATP content, and enhanced PINK1/Parkin-mediated mitophagy. These effects were partially blunted by siPINK1 or Mdivi-1. In HepG2 cells, curcumin improves insulin resistance by activating PINK1/Parkin-dependent mitophagy and rescuing mitochondrial function.</p>

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Curcumin ameliorates hepatic insulin resistance by activating PINK1/Parkin-mediated mitophagy

  • 期刊论文

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  • 发表日期：

    2026年4月8日

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  • Zhanhong Guo,
  • Huan Zhang,
  • Yinghong Kong

摘要

Insulin resistance (IR) is the key pathogenic factor of type 2 diabetes (T2DM) and its associated metabolic diseases. Mitochondrial dysfunction and inadequate mitophagy are central to this pathology. Curcumin, the main bioactive compound of Curcuma longa, has been reported to enhance insulin sensitivity, yet the mechanism in hepatocytes remains debated. Here we investigated whether curcumin alleviates hepatocyte IR by targeting PTEN-induced putative kinase 1 (PINK1)/ Parkin-dependent mitophagy. We induced IR in HepG2 cells with palmitic acid (PA) and then treated with curcumin. To verify the mechanism, we used PINK1 siRNA (siPINK1) and the mitophagy blocker Mdivi-1. Glucose uptake, glycogen content, lipid accumulation, phosphatidylinositol 3-kinase (PI3K)/ protein kinase B (Akt)/ glucose transporter 4 (GLUT4) signaling, mitochondrial function, and mitophagy markers were quantified by flow cytometry, glycogen assay kit, Oil Red O staining, confocal imaging, and Western blot. Curcumin mitigated PA-induced IR, increased PI3K/Akt phosphorylation and GLUT4 expression, promoted GLUT4 translocation to the plasma membrane, restored mitochondrial membrane potential and ATP content, and enhanced PINK1/Parkin-mediated mitophagy. These effects were partially blunted by siPINK1 or Mdivi-1. In HepG2 cells, curcumin improves insulin resistance by activating PINK1/Parkin-dependent mitophagy and rescuing mitochondrial function.