Evidence map›Paper›PMID 38032443›Full record

ArticleJournal of bioenergetics and biomembranes2024

Medium- and long-chain triglyceride propofol activates PI3K/AKT pathway and inhibits non-alcoholic fatty liver disease by inhibiting lipid accumulation.

Hui Liu, Mingshuo Hao, Wen Liu, Haiyan Chen, Changlong Han, Yun Shao, Liyuan Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Trial
  2. Article
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

7 authors at 2 institutions in 1 country.

Hui LiuDepartment of anesthesiology, Shidong Hospital, Affiliated to University of Shanghai for Science and Technology, Yangpu District, Shanghai, 200438, China.
Mingshuo HaoPathology Department, Jining NO.1 People's Hospital, 13 Jiankang Road, Rencheng District, Jining, Shandong, 272002, China.
Wen LiuDepartment of anesthesiology, Shidong Hospital, Affiliated to University of Shanghai for Science and Technology, Yangpu District, Shanghai, 200438, China.
Haiyan ChenDepartment of anesthesiology, Shidong Hospital, Affiliated to University of Shanghai for Science and Technology, Yangpu District, Shanghai, 200438, China.
Changlong HanDepartment of anesthesiology, Shidong Hospital, Affiliated to University of Shanghai for Science and Technology, Yangpu District, Shanghai, 200438, China.
Yun ShaoDepartment of anesthesiology, Shidong Hospital, Affiliated to University of Shanghai for Science and Technology, Yangpu District, Shanghai, 200438, China.
Liyuan WangDepartment of anesthesiology, Shidong Hospital, Affiliated to University of Shanghai for Science and Technology, Yangpu District, Shanghai, 200438, China. liyuanwang8101@hotmail.com.
University of Shanghai for Science and Technology · CNJining First People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease. The mechanism by which medium- and long-chain triglyceride (MCT/LCT) propofol plays a role in promoting NAFLD remains unclear. In this study, we investigated the effect of MCT/LCT propofol on NAFLD progression and its mechanism of action. In Huh-7 and HepG3 cells induced by free fatty acids (FFA), propofol downregulated the expression levels of TG and lipid metabolism-related proteins by promoting the activation of the PI3K/AKT pathway and suppressing FFA-induced lipid metabolic disorders. In a high-fat diet (HFD) -induced NAFLD mouse model, we demonstrated that propofol significantly inhibited liver steatosis, inflammatory cell infiltration, and fibrosis. In conclusion, our results suggest that MCT/LCT propofol reduces liver lipid accumulation by activating the PI3K/AKT pathway and further suppressing the NAFLD process.

Indexed as

Non-alcoholic Fatty Liver DiseasePropofolAnimalsDiet, High-FatLiverMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTriglyceridesPhosphatidylinositol 3-KinasesPropofolProto-Oncogene Proteins c-aktTriglyceridesLiver diseaseLiver steatosisMCT/LCTNAFLDPI3K/AKT

Identifiers

PMID38032443
OpenAlexW4389160734

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.