AI Article Synopsis
- The nutritional status in early life can have lasting effects on an animal's metabolism, potentially due to epigenetic changes, but more research is needed to fully understand this connection.
- Researchers used medaka fish to study the effects of a high-fat diet in early life, observing changes in liver tissue over time, including initial liver fat accumulation and significant alterations in gene expression and epigenetic modifications.
- The study found that while some epigenetic changes were reversible once a normal diet was introduced, others, particularly those linked to serious conditions like liver fibrosis and cancer, remained persistent, highlighting the complexity of how early nutrition can affect long-term health.
Article Abstract
Background: The nutritional status during early life can have enduring effects on an animal's metabolism, although the mechanisms underlying these long-term effects are still unclear. Epigenetic modifications are considered a prime candidate mechanism for encoding early-life nutritional memories during this critical developmental period. However, the extent to which these epigenetic changes occur and persist over time remains uncertain, in part due to challenges associated with directly stimulating the fetus with specific nutrients in viviparous mammalian systems.
Results: In this study, we used medaka as an oviparous vertebrate model to establish an early-life high-fat diet (HFD) model. Larvae were fed with HFD from the hatching stages (one week after fertilization) for six weeks, followed by normal chow (NC) for eight weeks until the adult stage. We examined the changes in the transcriptomic and epigenetic state of the liver over this period. We found that HFD induces simple liver steatosis, accompanied by drastic changes in the hepatic transcriptome, chromatin accessibility, and histone modifications, especially in metabolic genes. These changes were largely reversed after the long-term NC, demonstrating the high plasticity of the epigenetic state in hepatocytes. However, we found a certain number of genomic loci showing non-reversible epigenetic changes, especially around genes related to cell signaling, liver fibrosis, and hepatocellular carcinoma, implying persistent changes in the cellular state of the liver triggered by early-life HFD feeding.
Conclusion: In summary, our data show that early-life HFD feeding triggers both reversible and persistent epigenetic changes in medaka hepatocytes. Our data provide novel insights into the epigenetic mechanism of nutritional programming and a comprehensive atlas of the long-term epigenetic state in an early-life HFD model of non-mammalian vertebrates.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10441761 | PMC |
| http://dx.doi.org/10.1186/s12864-023-09557-1 | DOI Listing |
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