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Background <p>Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorder often accompanied by hepatic metabolic dysfunction. Short-term diabetes induces early hepatic alterations, including disrupted glucose and lipid metabolism, impaired insulin signaling, and inflammatory stress, rather than established NAFLD. These early changes may predispose the liver to progressive metabolic disease if persistent. This study aims to identify therapeutic targets by elucidating molecular and signaling pathways involved in diabetes-induced early hepatic metabolic disturbances, providing insights into initial liver responses and preventive intervention strategies.</p> Methods <p>A Venn diagram illustrated the overlapping targets, emphasizing the potential for targeted therapeutic intervention. Network pharmacology elucidated the strong interaction between protein-drug interactions, ultimately identifying nine key biomolecules: INSR, TGF-β, JNK, IKKβ, GSK3β, iNOS, GLUT4, SNAP23, and Syntaxin, which are crucial in the pathogenesis of both NAFLD-like metabolic state. Hesperidin (NF-HSP) is a promising therapeutic approach due to its ability to modulate insulin resistance and inflammatory pathways. To validate these findings, an animal model was employed, demonstrating that Nano-formulated hesperidin (NF-HSP) effectively ameliorated liver dysfunction induced by T2DM, as evidenced by biochemical parameters and liver function tests.</p> Results <p>Nano-formulated hesperidin exhibited antioxidant and anti-inflammatory properties, along with significant regulation of protein levels. Gene expression analysis corroborated these results, highlighting hesperidin’s role in mediating insulin resistance and IR/TGF-β1/GLUT4 signaling pathways.</p> Conclusion <p>This study provides strong evidence of the therapeutic potential of nano-hesperidin (NF-HSP) combined with nanotechnology in short-term diabetes-induced hepatic metabolic alterations, reducing NAFLD-like metabolic state, opening new possibilities for targeted intervention and treatment of these related metabolic diseases.</p>

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Mechanistic Evaluation of Nano-hesperidin in Attenuating Short-term Diabetes-induced Hepatic Dysfunction Through IR/TGF-β1/GLUT4 Signaling

  • 期刊论文

  • 发表日期：

    2026年3月21日

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  • Ritika Chauhan,
  • Nithya Ramesh,
  • Shazia Fathima Jaffer Hussain,
  • Selvam Rajendiran

摘要

Background

Type 2 diabetes mellitus (T2DM) is a prevalent metabolic disorder often accompanied by hepatic metabolic dysfunction. Short-term diabetes induces early hepatic alterations, including disrupted glucose and lipid metabolism, impaired insulin signaling, and inflammatory stress, rather than established NAFLD. These early changes may predispose the liver to progressive metabolic disease if persistent. This study aims to identify therapeutic targets by elucidating molecular and signaling pathways involved in diabetes-induced early hepatic metabolic disturbances, providing insights into initial liver responses and preventive intervention strategies.

Methods

A Venn diagram illustrated the overlapping targets, emphasizing the potential for targeted therapeutic intervention. Network pharmacology elucidated the strong interaction between protein-drug interactions, ultimately identifying nine key biomolecules: INSR, TGF-β, JNK, IKKβ, GSK3β, iNOS, GLUT4, SNAP23, and Syntaxin, which are crucial in the pathogenesis of both NAFLD-like metabolic state. Hesperidin (NF-HSP) is a promising therapeutic approach due to its ability to modulate insulin resistance and inflammatory pathways. To validate these findings, an animal model was employed, demonstrating that Nano-formulated hesperidin (NF-HSP) effectively ameliorated liver dysfunction induced by T2DM, as evidenced by biochemical parameters and liver function tests.

Results

Nano-formulated hesperidin exhibited antioxidant and anti-inflammatory properties, along with significant regulation of protein levels. Gene expression analysis corroborated these results, highlighting hesperidin’s role in mediating insulin resistance and IR/TGF-β1/GLUT4 signaling pathways.

Conclusion

This study provides strong evidence of the therapeutic potential of nano-hesperidin (NF-HSP) combined with nanotechnology in short-term diabetes-induced hepatic metabolic alterations, reducing NAFLD-like metabolic state, opening new possibilities for targeted intervention and treatment of these related metabolic diseases.