Journal of agricultural and food chemistryJan 27, 2026

Mulberry Leaf Alkaloids and 1-Deoxynojirimycin May Reduce Diet-Induced Fatty Liver Disease by Boosting Cell Cleanup through the PI3K/AKT/mTOR Pathway

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Feb 1, 2026

Abstract

1-Deoxynojirimycin (DNJ) significantly improves liver health in mice with metabolic-associated steatosis and hepatitis (MASH).

Mulberry leaf alkaloids (MLA) and DNJ alleviate liver injury, steatosis, inflammation, and fibrosis caused by a high-fat diet in MASH mice.
The protective effects of MLA and DNJ are linked to the inhibition of the PI3K/AKT/mTOR signaling pathway.
Activation of liver autophagy-related proteins is associated with the hepatoprotective effects of DNJ.
Molecular docking analysis indicates that DNJ has a strong binding affinity for PI3K, AKT, and mTOR.

Simplified

Alkaloid components derived from mulberry leaves exhibit regulatory potential for liver lipid metabolism abnormalities, oxidative stress, and inflammatory responses. Among these components, 1-Deoxynojirimycin (DNJ), the primary alkaloid compound, has various biological activities. This study focuses on exploring the hepatoprotective effects and potential mechanisms of mulberry leaf alkaloids (MLA) and DNJ on MASH. The results showed that MLA and DNJ can significantly improve the pathological changes in liver tissue induced by a choline-deficient, L-amino acid-defined, high-fat diet (CDAHFD), alleviating liver injury, steatosis, inflammation, and fibrosis in MASH mice. Subsequent research has indicated that this protective effect is associated with the inhibition of the PI3K/AKT/mTOR pathway and the activation of the expression of liver autophagy-related proteins. Additionally, molecular docking analysis and molecular dynamics simulation demonstrated that DNJ exhibited a good binding affinity with PI3K, AKT, and mTOR. In conclusion, DNJ promotes autophagy through the PI3K/AKT/mTOR pathway, thereby alleviating MASH symptoms and fibrosis in mice.

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Mulberry Leaf Alkaloids and 1-Deoxynojirimycin May Reduce Diet-Induced Fatty Liver Disease by Boosting Cell Cleanup through the PI3K/AKT/mTOR Pathway

Abstract

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