Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
The liver kinase B1 mediates the therapeutic efficacy of nuciferine against hepatic lipid accumulation in diabetic KKAy mice.
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Guo Yan, Chen Huijian, Li Tongqing, Huang Mi, Liu Pengxin, Mohammadtursun Nabijan, Kang Li, Aikemu Ainiwaer, Yang Xinzhou
Аннотация
BACKGROUND: Type-2 diabetes mellitus (T2DM) is a metabolic disorder characterized by insulin resistance (IR) and β-cell dysfunction. Nuciferine (NCF), derived from plants such as Nelumbo nucifera Gaertn., is an alkaloid with anti-obesity/T2DM effects. However, how NCF acts on hepatic lipid accumulation in T2DM treatment is not fully understood.
PURPOSE: This study aims to investigate how NCF reverses hepatic steatosis and treats T2DM through the LKB1/AMPK/mTOR pathway.
METHODS: High-fat diet-fed KK-Ay mice were used to establish an in vivo diabetic model. Insulin stimulation was used to establish hepatocyte models of IR.
RESULTS: We found that NCF reduced body weight and blood glucose levels in diabetic mice. NCF also decreased the number of lipid droplets and triglyceride levels in liver. Furthermore, NCF reduced the overexpression of p-mTOR and the lipogenesis-related protein in liver of diabetic mice, while it elevated the protein levels of p-LKB1, p-AMPK, and p-ACC. In HepG2-IR cells, NCF significantly inhibited lipid accumulation via the LKB1/AMPK/mTOR pathway. When LKB1 or AMPK antagonists were used or LKB1 was knocked down by siRNA, the inhibitory effect of NCF on lipid accumulation was blocked.
CONCLUSION: NCF inhibited hepatic lipid accumulation via the LKB1/AMPK/mTOR pathway, thereby contributing to the treatment of T2DM.
PURPOSE: This study aims to investigate how NCF reverses hepatic steatosis and treats T2DM through the LKB1/AMPK/mTOR pathway.
METHODS: High-fat diet-fed KK-Ay mice were used to establish an in vivo diabetic model. Insulin stimulation was used to establish hepatocyte models of IR.
RESULTS: We found that NCF reduced body weight and blood glucose levels in diabetic mice. NCF also decreased the number of lipid droplets and triglyceride levels in liver. Furthermore, NCF reduced the overexpression of p-mTOR and the lipogenesis-related protein in liver of diabetic mice, while it elevated the protein levels of p-LKB1, p-AMPK, and p-ACC. In HepG2-IR cells, NCF significantly inhibited lipid accumulation via the LKB1/AMPK/mTOR pathway. When LKB1 or AMPK antagonists were used or LKB1 was knocked down by siRNA, the inhibitory effect of NCF on lipid accumulation was blocked.
CONCLUSION: NCF inhibited hepatic lipid accumulation via the LKB1/AMPK/mTOR pathway, thereby contributing to the treatment of T2DM.
Предметные рубрики MeSH
AnimalsProtein Serine-Threonine KinasesLiverMaleAporphinesDiabetes Mellitus, Type 2MiceLipid MetabolismDiet, High-FatTOR Serine-Threonine KinasesDiabetes Mellitus, ExperimentalHumansNelumboAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesBlood GlucoseSignal TransductionHep G2 CellsInsulin ResistanceFatty LiverHypoglycemic Agents