Evidence map›Paper›PMID 42853441›Full record

ArticleFish physiology and biochemistry2026

PI3KC3/BECLIN1-dependent lipophagy mediates phosphorus-induced reduction of hepatic lipid deposition in hybrid yellow catfish.

Wu Hong Lv, Jia Li Jiang, Hui Min Sun, Mei Qin Zhuo

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Article in Fish physiology and biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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4 authors.

Wu Hong Lv *School of Fisheries, Ludong University, Yantai, 264025, China.
Jia Li Jiang *Hubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan, 430023, China.
Hui Min SunHubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan, 430023, China.
Mei Qin ZhuoHubei Key Laboratory of Animal Nutrition and Feed Science, School of Animal Science and Nutritional Engineering, Wuhan Polytechnic University, Wuhan, 430023, China. zmq@whpu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the molecular mechanism by which phosphorus (Pi) regulates hepatic lipid deposition in hybrid yellow catfish (Pelteobagrus fulvidraco × Pelteobagrus vachelli), a 56-day in vivo feeding trial was conducted with five dietary Pi levels: 0.54%, 0.65%, 0.74%, 0.98%, and 1.28%. Combined with in vitro incubation experiments using primary hepatocytes, this study focused on the PI3KC3/BECLIN1-mediated lipophagy pathway to assess hepatic morphology, expression of autophagy-related genes/proteins, and lipophagic activity. The results showed that hepatic morphology was intact in fish fed 0.65%-0.74% dietary Pi, whereas obvious vacuolization and lipid accumulation were observed in the 0.54% and 1.28% Pi groups. Pi levels of 0.74%-0.98% activated hepatic lipophagy and significantly upregulated the mRNA and protein expression of autophagy-related markers including PI3KC3, BECLIN1, and LC3B-II. In vitro experiments revealed that 2 mM Pi supplementation markedly reduced triglyceride (TG) content in oleic acid-induced hyperlipidemic hepatocytes, enhanced the protein expression of SLC20A1 and SLC20A2, promoted the physical interaction between PI3KC3 and BECLIN1, and strengthened lipid droplet-lysosome colocalization. These effects were significantly suppressed by the autophagy inhibitor 3-MA. In addition, Pi upregulated the expression of the hepatocellular Pi transporters SLC20A1 and SLC20A2 and induced a transient increase in intracellular free calcium ions. This study proposes a potential mechanism whereby Pi may initiate autophagy by promoting the binding of PI3KC3 to BECLIN1, thereby enhancing hepatic lipophagy and alleviating lipid deposition. These findings provide potential novel targets for the nutritional prevention and control of fatty liver disease in yellow catfish.

Indexed as

AutophagyBeclin-1CatfishesClass III Phosphatidylinositol 3-KinasesLipid MetabolismLiverPhosphorusAnimalsGene Expression RegulationHepatocytesBeclin-1Class III Phosphatidylinositol 3-KinasesPhosphorusHepatic lipid depositionHybrid yellow catfishLipophagyPhosphorusPI3KC3/BECLIN1

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.