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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Monkfish Peptides Mitigate High Fat Diet-Induced Hepatic Steatosis in Mice
Jiena Ye1, Xiaoxiao Tian1, Qiongfen Wang2
1Zhejiang Provincial Engineering Technology Research Center of Marine Biomedical Products, School of Food and Pharmacy, Zhejiang Ocean University, Zhoushan 316022, China.
Abstract:
Non-alcoholic fatty liver disease (NAFLD) is a hepatic metabolic syndrome usually accompanied by fatty degeneration and functional impairment. The aim of the study was to determine whether monkfish peptides (LPs) could ameliorate high-fat diet (HFD)-induced NAFLD and its underlying mechanisms. NAFLD was induced in mice by giving them an HFD for eight weeks, after which LPs were administered in various dosages. In comparison to the HFD control group: body weight in the LP-treated groups decreased by 23-28%; triacylglycerol levels in the blood decreased by 16-35%; and low-density lipoproteins levels in the blood decreased by 23-51%. Additionally, we found that LPs elevated the activity of hepatic antioxidant enzymes and reduced the inflammatory reactions within fatty liver tissue. Investigating the effect on metabolic pathways, we found that in LP-treated mice: the levels of phospho-AMP-activated protein kinase (p-AMPK), and phospho-acetyl CoA carboxylase (p-ACC) in the AMP-activated protein kinase (AMPK) pathway were up-regulated and the levels of downstream sterol regulatory element-binding transcription factor 1 (SREBP-1) were down-regulated; lipid oxidation increased and free fatty acid (FFA) accumulation decreased (revealed by the increased carnitine palmitoyltransferase-1 (CPT-1) and the decreased fatty acid synthase (FASN) expression, respectively); the nuclear factor erythroid-2-related factor 2 (Nrf2) antioxidant pathway was activated; and the levels of heme oxygenase-1 (HO-1) and nicotinamide quinone oxidoreductase 1 (NQO1) were increased. Overall, all these findings demonstrated that LPs can improve the antioxidant capacity of liver to alleviate NAFLD progression mainly through modulating the AMPK and Nrf2 pathways, and thus it could be considered as an effective candidate in the treatment of human NAFLD.
Insights
Monkfish peptides (LPs) effectively treat non-alcoholic fatty liver disease (NAFLD) by reducing body weight and improving liver health. LPs enhance antioxidant capacity and modulate key metabolic pathways, offering a promising therapeutic candidate for NAFLD.
Area of Science:
- Metabolic disease research
- Hepatology
- Nutraceutical science
Background:
- Non-alcoholic fatty liver disease (NAFLD) is a growing global health concern characterized by hepatic fat accumulation and inflammation.
- Current treatments for NAFLD are limited, necessitating the exploration of novel therapeutic agents.
- High-fat diets (HFDs) are a primary driver of NAFLD, making them a key model for studying disease mechanisms and interventions.
Purpose of the Study:
- To investigate the efficacy of monkfish peptides (LPs) in ameliorating high-fat diet-induced non-alcoholic fatty liver disease (NAFLD) in a mouse model.
- To elucidate the underlying molecular mechanisms by which LPs exert their protective effects against NAFLD.
- To evaluate the impact of LPs on key metabolic and antioxidant pathways implicated in NAFLD pathogenesis.
Main Methods:
- Induction of NAFLD in mice using a standardized high-fat diet (HFD) for eight weeks.
- Administration of varying dosages of monkfish peptides (LPs) to HFD-fed mice.
- Biochemical analysis of blood parameters (triacylglycerol, LDL), hepatic enzyme activity, and gene/protein expression related to metabolic and antioxidant pathways (AMPK, Nrf2).
Main Results:
- LP treatment significantly reduced body weight, blood triacylglycerol, and low-density lipoprotein levels compared to the HFD control group.
- LPs enhanced hepatic antioxidant enzyme activity and reduced inflammatory markers in liver tissue.
- LP administration upregulated the AMPK pathway (p-AMPK, p-ACC) and the Nrf2 antioxidant pathway (HO-1, NQO1), while downregulating SREBP-1 and decreasing lipid accumulation (increased CPT-1, decreased FASN).
Conclusions:
- Monkfish peptides (LPs) demonstrate significant potential in alleviating HFD-induced NAFLD in mice.
- LPs improve liver health by enhancing antioxidant capacity and modulating crucial metabolic pathways, primarily through the AMPK and Nrf2 signaling.
- These findings suggest that LPs could serve as a valuable therapeutic candidate for managing human non-alcoholic fatty liver disease.
