Evidence map›Paper›PMID 37764494›Full record

ArticleMolecules (Basel, Switzerland)2023

The Different Mechanisms of Lipid Accumulation in Hepatocytes Induced by Oleic Acid/Palmitic Acid and High-Fat Diet.

Miao Zhang, Xue Bai, Qian Du, Jiaojiao Xu, Danqing Wang, Lei Chen, Keting Dong, Ziyue Chen, Jianhong Yang

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 35 citations in OpenAlex.

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  19. miRNA-642a-3p protects β cells from glucolipotoxicity.Molecular therapy. Nucleic acids · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Miao ZhangSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Xue BaiSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Qian DuSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Jiaojiao XuSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Danqing WangSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Lei ChenSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Keting DongSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
Ziyue ChenSchool of Nursing, Capital Medical University, Beijing 100069, China.
Jianhong YangSavaid Medical School, University of Chinese Academy of Sciences, Beijing 101400, China.
University of Chinese Academy of Sciences · CNCapital Medical University · CN

Funding

the Fundamental Research Funds for the Central Universities Grant No. E2E43202X2
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the primary chronic liver disease worldwide, mainly manifested by hepatic steatosis. Hepatic lipids may be derived from dietary intake, plasma free fatty acid (FFA) uptake, or hepatic de novo lipogenesis (DNL). Currently, cellular and animal models of hepatocellular steatosis are widely used to study the pathogenesis of NAFLD and to investigate therapeutic agents. However, whether there are differences between the in vivo and in vitro models of the mechanisms that cause lipid accumulation has not been reported. We used OA/PA-induced NCTC 1469 cells and high-fat-diet-fed C57BL/6J mice to simulate a hepatocyte steatosis model of NAFLD and to detect indicators related to FFA uptake and DNL. In addition, when serological indicators were analysed in the mouse model, it was found that serum FASN levels decreased. The results revealed that, in the cellular model, indicators related to DNL were decreased, FASN enzyme activity was unchanged, and indicators related to FFA uptake were increased, including the high expression of CD36; while, in the animal model, indicators related to both FFA uptake and de novo synthesis were increased, including the high expression of CD36 and the increased protein levels of FASN with enhanced enzyme activity. In addition, after an analysis of the serological indicators in the mouse model, it was found that the serum levels of FASN were reduced. In conclusion, the OA/PA-induced cellular model can be used to study the mechanism of FFA uptake, whereas the high-fat-diet-induced mouse model can be used to study the mechanism of FFA uptake and DNL. Combined treatment with CD36 and FASN may be more effective against NAFLD. FASN in the serum can be used as one of the indicators for the clinical diagnosis of NAFLD.

Indexed as

Non-alcoholic Fatty Liver DiseaseOleic AcidAnimalsCD36 AntigensDiet, High-FatDisease Models, AnimalFatty Acids, NonesterifiedHepatocytesMiceMice, Inbred C57BLPalmitic AcidCD36 AntigensFatty Acids, NonesterifiedOleic AcidPalmitic Acidanimal modelsCD36cellular modelsde novo lipogenesisFASNfatty acid uptakeHFDlipid accumulationNAFLDoleic acid and palmitic acid

Identifiers

PMID37764494
PMCPMC10536454
OpenAlexW4386884974

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.