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Cited by 3Liver Disease Diagnosis and TreatmentLipid metabolism and biosynthesisPeroxisome Proliferator-Activated Receptors

Oleic Acid Increases Lipid Accumulation in Duck Hepatocytes by Promoting Apolipoprotein A1 Expression

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Pan, Ziyi, Li, Xuewen, Wu, Dongsheng, Xie, Longfei, Chen, Xingyong, Geng, Zhaoyu·2025·Animals
DOI 10.3390/ani15243603PMC PMC12729497
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Abstract

Background: Lipid overaccumulation in the liver predisposes ducks to metabolic disorders. The molecular mechanism of oleic acid (OA)-induced hepatic steatosis in ducks is not fully elucidated. Methods: A cellular model of steatosis was established by treating primary duck hepatocytes with OA. Transcriptome sequencing was performed to identify key signaling pathways and candidate genes. The role of Apolipoprotein A1 (APOA1) was investigated through overexpression and knockdown experiments. Intracellular triglycerides (TGs) were quantified commercially; lipid droplets were visualized by Oil Red O staining. Results: Intracellular TG accumulation was induced by OA treatment in a dose-dependent manner. Through transcriptome analysis, 1045 differentially expressed genes (DEGs) were identified, with APOA1 being recognized as a key candidate within the peroxisome proliferator-activated receptor (PPAR) signaling pathway. The content of TGs and lipid droplets was increased by APOA1 overexpression, whereas these effects were suppressed by APOA1 knockdown. The expression of acetyl-CoA carboxylase alpha (ACACA) and fatty acid synthase (FASN) was upregulated by APOA1. Conversely, the expression of carnitine O-palmitoyltransferase 1 (CPT1), acyl-CoA oxidase 1 (ACOX1), and apolipoprotein B (APOB) was downregulated. Conclusions: This study demonstrates that OA upregulates APOA1, suggesting the involvement of the PPAR pathway and providing a theoretical basis for modulating hepatic fat deposition.

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  • Oleic acid primarily promotes the formation of larger lipid droplets and facilitates the safe esterification of fatty acids into triglycerides, whereas palmitic acid is more strongly associated with mitochondrial fragmentation, increased oxidative metabolism, and ROS formation in both the cytosol and mitochondria.

    “Oleic acid primarily promotes the formation of larger lipid droplets and facilitates the safe esterification of fatty acids into triglycerides [148,149,150,151], whereas palmitic acid is more strongly associated with mitochondrial fragmentation, increased oxidative metabolism, and ROS formation in both the cytosol and mitochondria.”

    From The HepG2 Cell Line as a Model for Studying Metabolic Dysfunction-Associated Steatotic Liver Disease (2026) · cites this paper as [150]

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Authors
Pan, Z., Li, X., Wu, D., Xie, L., Chen, X., & Geng, Z.
Affiliations
  • Chinese Academy of Tropical Agricultural Sciences (CN)
  • Anhui Agricultural University (CN)
Corresponding author
Geng, Zhaoyu
ORCID
Venue
Animals
Publisher
MDPI AG
Published
2025-12-15
Volume
15
Issue
24
Pages
3603
ISSN
2076-2615 (ISSN-L)
DOI
10.3390/ani15243603
PMC
PMC12729497
OpenAlex
W4417328233
Cited by
3
References
35
Citations by year
2026: 3
FWCI
2.08
Type
journal article
Language
en
Open access
Licence
Locations
  • Animals (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Major Scientific and Technological Special Project in Anhui Province (201903a06020018)
  • Jiangsu Outstanding Postdoctoral Fellowship (2024ZB42)
  • University Synergy Innovation Program of Anhui Province (GXXT-2021-052)
Topics
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
Keywords
oleic acid, hepatic steatosis, apolipoprotein A-I, PPAR signaling, lipid accumulation, triglyceride accumulation, lipid droplets, fatty acid synthase, ACACA, ACOX1, apolipoprotein B

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