ArticleNutrition & metabolism2023
High fat diet and PCSK9 knockout modulates lipid profile of the liver and changes the expression of lipid homeostasis related genes.
Article in Nutrition & metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Roles of proprotein convertase subtilisin/kexin type 9 (PCSK9) in the regulation of hepatic triglyceride metabolism.Journal of lipid research · 2026Review
- From cooperation to collapse: the diet-microbiota-host gene triad in disease and aging.Frontiers in microbiomes · 2026Review
- AI-driven identification of nutrition-modulated biomarkers and drug targets for cardiovascular therapeutic mechanisms.Frontiers in pharmacology · 2026Review
- Mechanisms of action and therapeutic potential of PCSK9-regulating drugs.Pharmaceutical biology · 2025Review
- Article
- Gut-Liver Axis-Mediated Anti-Obesity Effects and Viscosity Characterization of a Homogenized Viscous Vegetable Mixture in Mice Fed a High-Fat Diet.Plants (Basel, Switzerland) · 2025Article
- Article
- Reduced circulating CD63Cardiovascular diabetology · 2024Article
- A novel small-molecule PCSK9 inhibitor E28362 ameliorates hyperlipidemia and atherosclerosis.Acta pharmacologica Sinica · 2024Article
- Exserolide J ameliorates lipid accumulationHeliyon · 2024Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundHigh fat diet (HFD) increases the likelihood of dyslipidemia, which can be a serious risk factor for atherosclerosis, diabetes or hepatosteatosis. Although changes in different blood lipid levels were broadly investigated, such alterations in the liver tissue have not been studied before. The aim of the current study was to investigate the effect of HFD on hepatic triglyceride (TG), diglyceride (DG) and ceramide (CER) levels and on the expression of four key genes involved in lipid homeostasis (Pcsk9, Ldlr, Cd36 and Anxa2) in the liver. In addition, the potential role of PCSK9 in the observed changes was further investigated by using PCSK9 deficient mice.
methodsWe used two in vivo models: mice kept on HFD for 20 weeks and PCSK9
resultsIn HFD mice, hepatic PCSK9 expression was decreased and ANXA2 expression was increased both on mRNA and protein levels, and the amount of LDLR and CD36 receptor proteins was increased. While LDLR protein level was also elevated in the livers of PCSK9
conclusionsOur results show that obesogenic HFD downregulates PCSK9 expression in the liver and causes alterations in the hepatic lipid accumulation, which resemble those observed in PCSK9 deficiency. These findings suggest that PCSK9-mediated modulation of LDLR and CD36 expression might contribute to the HFD-induced changes in lipid homeostasis.
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