article · Antioxidants
Liposome-encapsulated berberine offers a potential therapeutic approach for treating liver damage associated with advanced type 2 diabetes. In an experimental rat model, administering liposomal berberine restored damaged liver tissue microarchitectures, decreased hepatic steatosis, and aided the regulation of lipid metabolism. The intervention also increased glucagon-like peptide-1 expression, which supported insulin biosynthesis. At the cellular level, the treatment promoted protective autophagy by activating LC3-II and Beclin-1 proteins via the AMPK/mTOR signalling pathway. In addition, liposomal berberine reduced endoplasmic reticulum stress by limiting the expression of CHOP and JNK, while simultaneously curbing oxidative stress and inflammation in the liver tissue. These mechanisms collectively alleviated diabetic liver injury in the tested animal subjects.
Liver damage is a debilitating complication in advanced type 2 diabetes, presenting a major challenge for long-term disease management. Demonstrating that liposome-encapsulated berberine can restore tissue structure, boost insulin-related signalling, and activate protective cellular recycling pathways provides important biological insights. This knowledge aids researchers working on targeted therapies to prevent severe organ decline and metabolic distress in diabetic patients.
This research could inform the development of encapsulated nutraceutical or pharmaceutical therapies targeting non-alcoholic fatty liver changes and hepatic complications in type 2 diabetes. The findings are primarily relevant to pharmaceutical formulation developers and metabolic disease researchers. Because the evidence is limited to an animal model, the technology remains at an early laboratory stage, requiring extensive pharmacokinetics, safety testing, and clinical trials before any real-world healthcare application.
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In the advanced stages of type 2 diabetes mellitus (T2DM), diabetic liver damage is a common complication that can devastate a patient's quality of life. The present study investigated the ability of liposomal berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM) and the possible pathways by which it does so. Liver tissue microarchitectures and immunohistochemical staining were applied during the study. The rats were divided into a control non-diabetic group and four diabetic groups, which are the T2DM, T2DM-Lip-BBR (10 mg/kg b.wt), T2DM-Vildagliptin (Vild) (10 mg/kg b.wt), and T2DM-BBR-Vild (10 mg/kg b.wt + Vild (5 mg/kg b.wt) groups. The findings demonstrated that Lip-BBR treatment could restore liver tissue microarchitectures, reduce steatosis and liver function, and regulate lipid metabolism. Moreover, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats. Lip-BBR also activated the GLP-1 expression, which stimulated insulin biosynthesis. It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation. Collectively, Lip-BBR ameliorated diabetic liver injury in a T2DM rat model with its promotion activity of AMPK/mTOR-mediated autophagy and limiting ER stress.
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DOI: 10.3390/antiox12061220
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