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<p>A high-fat diet (HFD) can lead to non-alcoholic fatty liver disease (NAFLD) by lipid accumulation in the liver. In this study, we investigated hepatic lipid content, microRNA (miRNA) expression pattern, and potential alterations in gene and protein expression in the livers of mice fed with HFD for 16&#xa0;weeks. Liver lipid content was assayed with colorimetric assay kits. The miRNA target genes were predicted using the TargetScan and miRBase databases. MicroRNA profile and transcriptional changes in lipid metabolism-related genes were analyzed using quantitative real-time PCR, and protein expressions were determined by Western blot analysis. Mice that were fed with a high-fat diet showed a significant increase in hepatic triglycerides and total cholesterol, along with considerable up-regulation of mmu-miR-199a-5p and down-regulation of mmu-miR-130a-3p, mmu-miR-200a-3p, mmu-miR-7002-5p, mmu-miR-145a-5p, and mmu-miR-101a-3p. Mice fed a high-fat diet experienced an increase in peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer binding protein alpha (CEBPα), sterol regulatory element binding transcription factor 1 (SREBP1), fatty acid synthase (FASN), and fatty acid binding protein 4 (FABP4) transcriptional levels, which was counteracted by a decrease in sirtuin1 levels. Furthermore, we discovered that mice given a high-fat diet had higher levels of PPARγ, CEBPα, and SREBP1, with lower levels of sirtuin1 proteins. In conclusion, alterations in the liver miRNA profile and miRNA-targeted genes associated with lipid metabolism are a consequence of high-fat dietary intake. Potential endogenous modulators of NAFLD pathogenesis, such as miRNAs, may eventually offer novel therapeutic intervention strategies.</p>

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Hepatic miRNA Expression Pattern and Changes in Lipid Metabolism-Related Genes in Mice Fed a High-Fat Diet for 16 Weeks

  • 期刊论文

  • 发表日期：

    2025年9月17日

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  • Ahmet Cumaoğlu,
  • Güzide Şatir Başaran

摘要

A high-fat diet (HFD) can lead to non-alcoholic fatty liver disease (NAFLD) by lipid accumulation in the liver. In this study, we investigated hepatic lipid content, microRNA (miRNA) expression pattern, and potential alterations in gene and protein expression in the livers of mice fed with HFD for 16 weeks. Liver lipid content was assayed with colorimetric assay kits. The miRNA target genes were predicted using the TargetScan and miRBase databases. MicroRNA profile and transcriptional changes in lipid metabolism-related genes were analyzed using quantitative real-time PCR, and protein expressions were determined by Western blot analysis. Mice that were fed with a high-fat diet showed a significant increase in hepatic triglycerides and total cholesterol, along with considerable up-regulation of mmu-miR-199a-5p and down-regulation of mmu-miR-130a-3p, mmu-miR-200a-3p, mmu-miR-7002-5p, mmu-miR-145a-5p, and mmu-miR-101a-3p. Mice fed a high-fat diet experienced an increase in peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer binding protein alpha (CEBPα), sterol regulatory element binding transcription factor 1 (SREBP1), fatty acid synthase (FASN), and fatty acid binding protein 4 (FABP4) transcriptional levels, which was counteracted by a decrease in sirtuin1 levels. Furthermore, we discovered that mice given a high-fat diet had higher levels of PPARγ, CEBPα, and SREBP1, with lower levels of sirtuin1 proteins. In conclusion, alterations in the liver miRNA profile and miRNA-targeted genes associated with lipid metabolism are a consequence of high-fat dietary intake. Potential endogenous modulators of NAFLD pathogenesis, such as miRNAs, may eventually offer novel therapeutic intervention strategies.