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Comparative study of palmitoleic acid, sea buckthorn oil, and lovastatin in hepatocellular steatosis model

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Szustak, Marcin, Pichlak, Marta, Korkus, Eliza, Kamińska, Daria, Koziołkiewicz, Maria, Dąbrowski, Grzegorz, Czaplicki, Sylwester, Konopka, Iwona, Gendaszewska-Darmach, Edyta·2026·Scientific Reports
DOI 10.1038/s41598-026-37006-yPMC PMC12902076
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Abstract

Palmitoleic acid (POA) has been associated with various metabolic effects, including regulating lipid metabolism and cholesterol production. In this study, we explored the impact of both cis - (cPOA) and trans -palmitoleic acid (tPOA), along with sea buckthorn oil (SBO), a natural source rich in cPOA, on lipid content, metabolic activity, and Rap1 prenylation in HepG2 cells. We employed a free fatty acids-induced steatosis model. Our findings revealed that neither cPOA, tPOA, SBO, nor digested SBO impaired the metabolic activity of HepG2 cells, even under steatotic conditions. All treatments led to triacylglycerol (TAG) accumulation, with tPOA demonstrating the beneficial effect. While cholesterol levels remained unchanged in normal cells, a reduction was noted in steatotic cells, comparable to the effect of lovastatin. Molecular docking suggested that both POA isomers may bind and block the catalytic pocket of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). To further explore this, we examined their influence on Rap1 prenylation and subcellular localization. Under steatotic conditions, both POA isomers, particularly at concentrations of 50 and 100 µM, elevated cytosolic Rap1 levels, whereas no significant changes were observed in membrane or cytosolic Rap1a protein levels in normal HepG2 cultures. Notably, unlike lovastatin, POA isomers and digested SBO enhanced glucose-stimulated insulin secretion from pancreatic cells. Our results highlight the potential of POA isomers and SBO as modulators of lipid metabolism, cholesterol production, and insulin secretion, suggesting their relevance in managing metabolic disorders.

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Fig. 1 Impact of a mixture of palmitic acid (PA) and oleic acid (OA) used at various concentrations on lipid accumulation and viability in HepG2 cells. A: Representative images of HepG2 cells stained with Nile Red, captured under both visible and fluorescent light (Ex: 482/35, Em: 536/40). B: Cellular viability assessed after 24-h incubation with PA/OA mixtures. C: Quantitative analysis of intracellular lipid content using Nile Red staining. D: TAG accumulation in control and steatotic cells (300 µM PA/OA) measured with Triglyceride Colorimetric Assay Kit. The results are representative of at least five independent biological replicates (n = 5). The bars represent the means ± SEM. ***p < 0.001, ****p < 0.0001 versus control. Images of HepG2 cells under visible and fluorescent light (Ex: 482/35, Em: 536/40). cPOA, cis-palmitoleic acid; FFA, free fatty acid; SBO, sea buckthorn oil; TAG, triacylglycerol; tPOA, trans-palmitoleic acid.
Fig. 1 Impact of a mixture of palmitic acid (PA) and oleic acid (OA) used at various concentrations on lipid accumulation and viability in HepG2 cells. A: Representative images of HepG2 cells stained with Nile Red, captured under both visible and fluorescent light (Ex: 482/35, Em: 536/40). B: Cellular viability assessed after 24-h incubation with PA/OA mixtures. C: Quantitative analysis of intracellular lipid content using Nile Red staining. D: TAG accumulation in control and steatotic cells (300 µM PA/OA) measured with Triglyceride Colorimetric Assay Kit. The results are representative of at least five independent biological replicates (n = 5). The bars represent the means ± SEM. ***p < 0.001, ****p < 0.0001 versus control. Images of HepG2 cells under visible and fluorescent light (Ex: 482/35, Em: 536/40). cPOA, cis-palmitoleic acid; FFA, free fatty acid; SBO, sea buckthorn oil; TAG, triacylglycerol; tPOA, trans-palmitoleic acid.CC BY · PubMed Central
Fig. 2 Effects of cPOA, tPOA, SBO, and digested SBO on viability and lipid accumulation in control and FFA-induced steatostic HepG2 cells. A: Viability of control cells treated with increasing concentrations (5–100 µM) of the tested compounds. For SBO, concentrations were adjusted based on POA content. B: Viability of cells with FFA-induced steatosis (300 µM PA/OA) following treatment with the same concentration range of compounds. Viability was assessed at 24 (A1, B1), 48 (A2, B2), and 72 (A3, B3) hours; bar shading intensity corresponds to increasing concentrations: 5, 10, 25, 50, and 100 µM. C: Quantitative detection of lipid accumulation in control cells using Nile Red fluorescence staining. D: Quantitative detection of lipids with Nile Red staining in steatosis-induced cells (300 µM PA/OA). E: TAG accumulation in control cells measured with a Triglyceride Colorimetric Assay Kit. F: TAG accumulation in steatotic cells measured with a Triglyceride Colorimetric Assay Kit. Nile Red staining and TAG detection were conducted after 24 h of incubation with the tested compounds. Data represent at least 8 independent biological replicates (n = 8). The bars represent the means ± SEM. **p < 0.01, ***p < 0.001, ****p < 0.0001 versus control. cPOA, cis-palmitoleic acid; FFA, free fatty acid; OA/PA, oleic acid/palmitic acid; SBO, sea buckthorn oil; TAG, triacylglycerol; tPOA, trans-palmitoleic acid.
Fig. 2 Effects of cPOA, tPOA, SBO, and digested SBO on viability and lipid accumulation in control and FFA-induced steatostic HepG2 cells. A: Viability of control cells treated with increasing concentrations (5–100 µM) of the tested compounds. For SBO, concentrations were adjusted based on POA content. B: Viability of cells with FFA-induced steatosis (300 µM PA/OA) following treatment with the same concentration range of compounds. Viability was assessed at 24 (A1, B1), 48 (A2, B2), and 72 (A3, B3) hours; bar shading intensity corresponds to increasing concentrations: 5, 10, 25, 50, and 100 µM. C: Quantitative detection of lipid accumulation in control cells using Nile Red fluorescence staining. D: Quantitative detection of lipids with Nile Red staining in steatosis-induced cells (300 µM PA/OA). E: TAG accumulation in control cells measured with a Triglyceride Colorimetric Assay Kit. F: TAG accumulation in steatotic cells measured with a Triglyceride Colorimetric Assay Kit. Nile Red staining and TAG detection were conducted after 24 h of incubation with the tested compounds. Data represent at least 8 independent biological replicates (n = 8). The bars represent the means ± SEM. **p < 0.01, ***p < 0.001, ****p < 0.0001 versus control. cPOA, cis-palmitoleic acid; FFA, free fatty acid; OA/PA, oleic acid/palmitic acid; SBO, sea buckthorn oil; TAG, triacylglycerol; tPOA, trans-palmitoleic acid.CC BY · PubMed Central
Fig. 3 Effects of cPOA, tPOA, SBO, and digested SBO on intracellular cholesterol content (A, B) and HMGCR gene expression (C, D) in control (A, C) and FFA-induced steatotic (B, D) HepG2 cells. Cells were exposed to indicated concentrations of compounds or 5 µM lovastatin. Results represent at least 3 independent biological samples with 3 repeats each (n = 3). The bars represent the means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 versus control. βACT, β-aktyna; cPOA, cis-palmitoleic acid; FFA, free fatty acid; OA/PA, oleic acid/palmitic acid; SBO, sea buckthorn oil; tPOA, trans-palmitoleic acid.
Fig. 3 Effects of cPOA, tPOA, SBO, and digested SBO on intracellular cholesterol content (A, B) and HMGCR gene expression (C, D) in control (A, C) and FFA-induced steatotic (B, D) HepG2 cells. Cells were exposed to indicated concentrations of compounds or 5 µM lovastatin. Results represent at least 3 independent biological samples with 3 repeats each (n = 3). The bars represent the means ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 versus control. βACT, β-aktyna; cPOA, cis-palmitoleic acid; FFA, free fatty acid; OA/PA, oleic acid/palmitic acid; SBO, sea buckthorn oil; tPOA, trans-palmitoleic acid.CC BY · PubMed Central
Fig. 4 Molecular docking of cPOA, tPOA, HMGCoA, and lovastatin acid into HMGCoA reductase. Mean score and energy value were presented with the means ± SD from at least 10 experiments. The location of the molecule in the catalytic pocket, with the most important amino acid residues within the binding pocket, is shown on the bottom. The neighbouring amino acid residues are listed in the table, with those forming hydrogen bonds with the molecule highlighted in green. cPOA, cis-palmitoleic acid; HMG-CoA, 3-hydroxy-3-methylglutaryl coenzyme A; LOV ACID, lovastatin acid; tPOA, trans-palmitoleic acid.
Fig. 4 Molecular docking of cPOA, tPOA, HMGCoA, and lovastatin acid into HMGCoA reductase. Mean score and energy value were presented with the means ± SD from at least 10 experiments. The location of the molecule in the catalytic pocket, with the most important amino acid residues within the binding pocket, is shown on the bottom. The neighbouring amino acid residues are listed in the table, with those forming hydrogen bonds with the molecule highlighted in green. cPOA, cis-palmitoleic acid; HMG-CoA, 3-hydroxy-3-methylglutaryl coenzyme A; LOV ACID, lovastatin acid; tPOA, trans-palmitoleic acid.CC BY · PubMed Central
Fig. 5 Effect of cPOA, tPOA, SBO, and SBO digested on Rap1A prenylation in HepG2 cells. Control (A, B and E, F) and FFA-induced steatotic cells (C, D and G, H) were exposed to indicated concentrations of compounds or 5 µM lovastatin (Lov) for 48 h. Subsequently, cells were lysed and isolation of cytosolic and membrane proteins was performed. Cytosolic fractions containing unprenylated proteins were western blotted for Rap1A and β-actin (A, C and E, G), and the immunoblot bands were quantified by densitometry analysis, normalized to β-actin, and presented as a percentage of controls (B, D and F, H). Lovastatin was used as a positive control. Treatment of cells with lovastatin should prevent the Rap1A accumulation at the membrane. Data represented mean ± SEM from at least three independent experiments (n = 3); *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001. Cropped gels are presented here; full-length gels and blots without cropping are included in the Supplementary Information file. cPOA, cis-palmitoleic acid; FFA, free fatty acid; OA/PA, oleic acid/palmitic acid; SBO, sea buckthorn oil; tPOA, trans-palmitoleic acid.
Fig. 5 Effect of cPOA, tPOA, SBO, and SBO digested on Rap1A prenylation in HepG2 cells. Control (A, B and E, F) and FFA-induced steatotic cells (C, D and G, H) were exposed to indicated concentrations of compounds or 5 µM lovastatin (Lov) for 48 h. Subsequently, cells were lysed and isolation of cytosolic and membrane proteins was performed. Cytosolic fractions containing unprenylated proteins were western blotted for Rap1A and β-actin (A, C and E, G), and the immunoblot bands were quantified by densitometry analysis, normalized to β-actin, and presented as a percentage of controls (B, D and F, H). Lovastatin was used as a positive control. Treatment of cells with lovastatin should prevent the Rap1A accumulation at the membrane. Data represented mean ± SEM from at least three independent experiments (n = 3); *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, and ****p ≤ 0.0001. Cropped gels are presented here; full-length gels and blots without cropping are included in the Supplementary Information file. cPOA, cis-palmitoleic acid; FFA, free fatty acid; OA/PA, oleic acid/palmitic acid; SBO, sea buckthorn oil; tPOA, trans-palmitoleic acid.CC BY · PubMed Central
Fig. 6 Effect of cPOA, tPOA, SBO, and SBO digested on glucose-stimulated insulin secretion (GSIS) in MIN6 cells. Cells were exposed to indicated concentrations of compounds or 5 µM lovastatin for 24 h. Data represented mean ± SEM from at least three independent experiments (n = 3); ####p ≤ 0.0001 versus 2 mM glucose control, ****p ≤ 0.0001 versus 20 mM glucose control. cPOA, cis-palmitoleic acid; SBO, sea buckthorn oil; tPOA, trans-palmitoleic acid.
Fig. 6 Effect of cPOA, tPOA, SBO, and SBO digested on glucose-stimulated insulin secretion (GSIS) in MIN6 cells. Cells were exposed to indicated concentrations of compounds or 5 µM lovastatin for 24 h. Data represented mean ± SEM from at least three independent experiments (n = 3); ####p ≤ 0.0001 versus 2 mM glucose control, ****p ≤ 0.0001 versus 20 mM glucose control. cPOA, cis-palmitoleic acid; SBO, sea buckthorn oil; tPOA, trans-palmitoleic acid.CC BY · PubMed Central
Fig. 7 Effects of POA isomers, digested sea buckthorn oil (SBO) and lovastatin on cholesterol synthesis, Rap1a activation, and insulin secretion. The left panel outlines the pathway from HMG-CoA reductase (HMGCR) expression through the mevalonate pathway to cholesterol synthesis and subsequent Rap1a activation in liver cells. The right panel details how different concentrations of cPOA, tPOA, SBO, and Lovastatin influence the prenylation status and subcellular localization of Rap1a (cytosolic inactive vs. membrane-bound active form). The bottom section connects these molecular events to physiological outcomes, showing the impact on hepatic gluconeogenesis and pancreatic insulin secretion (created by BioRender.com).
Fig. 7 Effects of POA isomers, digested sea buckthorn oil (SBO) and lovastatin on cholesterol synthesis, Rap1a activation, and insulin secretion. The left panel outlines the pathway from HMG-CoA reductase (HMGCR) expression through the mevalonate pathway to cholesterol synthesis and subsequent Rap1a activation in liver cells. The right panel details how different concentrations of cPOA, tPOA, SBO, and Lovastatin influence the prenylation status and subcellular localization of Rap1a (cytosolic inactive vs. membrane-bound active form). The bottom section connects these molecular events to physiological outcomes, showing the impact on hepatic gluconeogenesis and pancreatic insulin secretion (created by BioRender.com).CC BY · PubMed Central

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Metadata

Authors
Szustak, M., Pichlak, M., Korkus, E., Kamińska, D., Koziołkiewicz, M., Dąbrowski, G., Czaplicki, S., Konopka, I., & Gendaszewska-Darmach, E.
Affiliations
  • Lodz University of Technology (PL)
  • University of Warmia and Mazury in Olsztyn (PL)
ORCID
Venue
Scientific Reports
Publisher
Springer Science and Business Media LLC
Published
2026-01-24
Volume
16
Issue
1
Pages
6135-6135
ISSN
2045-2322 (ISSN-L)
DOI
10.1038/s41598-026-37006-y
PMC
PMC12902076
OpenAlex
W7125596720
Cited by
5
References
50
Citations by year
2026: 5
FWCI
52.97
Type
journal article
Language
en
Open access
Licence
Locations
  • Scientific Reports (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • PubMed Central (publishedVersion, cc-by)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
The National Science Centre, Poland (2018/31/B/NZ9/02433)
Topics
  • Health Sciences › Medicine › Complementary and alternative medicine › Phytochemical and Pharmacological Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
Keywords
palmitoleic acid, trans-palmitoleic acid, sea buckthorn oil, lovastatin, HepG2 cells, triglyceride accumulation, cholesterol, HMGCR, HMGR, glucose-stimulated insulin secretion, lipid metabolism, insulin secretion
MeSH terms
Cholesterol, Fatty Acids, Monounsaturated, Fatty Liver, Humans, Hydroxymethylglutaryl CoA Reductases, Lovastatin, Plant Oils, Triglycerides, Hippophae, Lipid Metabolism, Hep G2 Cells, Molecular Docking Simulation

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CoChat. (2026). Citation check: Comparative study of palmitoleic acid, sea buckthorn oil, and lovastatin in hepatocellular steatosis model. https://app.cochat.ai/papers/10.1038/s41598-026-37006-y
The paper
Szustak, M., Pichlak, M., Korkus, E., Kamińska, D., Koziołkiewicz, M., Dąbrowski, G., Czaplicki, S., Konopka, I., & Gendaszewska-Darmach, E. (2026). Comparative study of palmitoleic acid, sea buckthorn oil, and lovastatin in hepatocellular steatosis model. Scientific Reports. https://doi.org/10.1038/s41598-026-37006-y