Evidence map›Paper›PMID 41415834›Full record

ArticleFrontiers in nutrition2025

Identification of the role of sugar-sweetened beverages in the progression of a murine metabolic dysfunction-associated steatotic liver disease model.

Yong-Qiang Li, Chen Huang, Jiawei Chen, Siqi Yang, Jiemin Cheng, Huiting Chen, Yongjian Zhou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
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  3. Review
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.

Yong-Qiang Li *Department of Gastroenterology, The First Affiliated Hospital, The First Clinical Medical School, Jinan University, Guangzhou, China.
Chen Huang *Department of Gastroenterology and Hepatology, Guangzhou Key Laboratory of Digestive Diseases, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Jiawei Chen *Department of Gastroenterology and Hepatology, Guangzhou Key Laboratory of Digestive Diseases, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Siqi YangDepartment of Gastroenterology and Hepatology, Guangzhou Key Laboratory of Digestive Diseases, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Jiemin ChengDepartment of Gastroenterology and Hepatology, Guangzhou Key Laboratory of Digestive Diseases, Guangzhou Digestive Disease Center, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Guangzhou, China.
Huiting ChenDepartment of Gastroenterology, The First Affiliated Hospital, The First Clinical Medical School, Jinan University, Guangzhou, China.
Yongjian ZhouDepartment of Gastroenterology, The First Affiliated Hospital, The First Clinical Medical School, Jinan University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Rising metabolic dysfunction-associated steatotic liver disease (MASLD) prevalence parallels increased sugar-sweetened beverage (SSB) consumption. Clinical studies suggest differential metabolic effects of fructose, glucose, and sucrose, yet their distinct roles in MASLD pathogenesis remain uncharacterized in preclinical models. This study aimed to establish a murine model to dissect the specific contributions of fructose, glucose, and sucrose to MASLD progression. Methods: This study establishes a murine model to dissect SSB-specific contributions to MASLD progression. Eight-week-old male C57BL/6N mice were fed a high-fat high-cholesterol (HFHC) diet with/without fructose-, glucose-, or sucrose-sweetened beverages for 10 weeks. Hepatic transcriptomic profiles were analyzed via microarray, followed by functional enrichment. Protein-protein interaction (PPI) network and single-cell analysis identify pathway perturbations and hub genes. Results: Fructose-SB supplementation, unlike glucose or sucrose, exacerbated HFHC-induced MASLD phenotypes, including elevated body weight, hepatic steatosis, glucose intolerance, and hepatocellular injury. Transcriptomics identified 2,195 fructose-specific differentially expressed genes (DEGs: 1,978 upregulated, 224 downregulated). Upregulated DEGs were enriched in thyroid hormone signaling, lysosomal activity, and autophagy, while downregulated DEGs implicated oxidative phosphorylation suppression. PPI analysis revealed key hub genes (Akt1, Stat3, Ctnnb1, Ep300) and mitochondrial components (mt-Nd4, mt-Cytb, Uqcrq) as central regulators of fructose-driven pathology. Fructose-SB uniquely accelerates MASLD progression in HFHC-fed mice through transcriptional reprogramming of metabolic and mitochondrial pathways. In mice fed a high-fructose diet, expression of key hub genes was elevated, particularly in Kupffer and endothelial cells, which were also enriched in proportion. These findings highlight fructose-specific mechanisms in MASLD pathogenesis and identify potential therapeutic targets for SSB-associated metabolic disorders.

Indexed as

bioinformatics analysisdietary interventionsfructoseMASLDsugar-sweetened beverages

Identifiers

PMID41415834
PMCPMC12708248

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