ArticleBMC gastroenterology2026
Energy metabolism alteration and gene expression reprogramming in a cell model of high fat load non-alcoholic fatty liver disease.
Article in BMC gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
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Authors and funding
10 authors.
Funding
Abstract
backgroundMetabolic rewiring plays a crucial role in the energy metabolism of hepatocytes during steatosis. However, the precise alterations in energy metabolism remain unclear. The aim of this study was to investigate the effects of lipid exposure on cellular energy metabolism and gene expression in a cellular model of non-alcoholic fatty liver disease (NAFLD). METHODS AND
resultsWe induced hepatocyte steatosis in the hepatocyte cell line Huh7 via treatment with high levels of palmitate and oleate for 24 h. We then analysed transcriptomics, proteomics, mitochondrial phenotypes, and cellular energy metabolism. Fatty acid-treated cells presented significant accumulation of lipid droplets and reduced viability. Real-time bioenergetics analyses demonstrated a shift towards mitochondrial respiration for energy production, accompanied by a reduction in glycolytic adenosine triphosphate (ATP) production. However, the overall rate of ATP production remained constant. RNA-seq analysis revealed altered expression of 149 transcripts associated with lipid storage and catabolism, whereas 172 proteins presented significantly altered levels and were enriched in RNA processing and splicing functions. Two genes, ACAA2 and PLIN2, were significantly altered at both the transcript and protein levels and may be crucial for maintaining mitochondrial function in early non-alcoholic fatty liver (NAFL).
conclusionsOur NAFLD model demonstrated that the reprogramming of genes involved in lipid storage and catabolism is crucial for early NAFL pathogenesis development. This study offers new insights with valuable implications for designing future research into novel therapeutic strategies.
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