International Journal of Molecular Sciences · 6 authors, 4 centres
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In a rat model, neonatal lactose intolerance (NLI) triggered by lactase overloading caused long-term growth retardation, cardiomyocyte hyperpolyploidy, and transcriptomic changes resembling cardiac pathologies. The study suggests NLI may be a trigger for developmental programming of adult cardiovascular disease.
This preclinical study used a rat model of neonatal lactose intolerance (NLI) induced by lactase overloading. The researchers evaluated long-term effects on cardiomyocyte ploidy, DNA damage, and transcriptome via cytophotometry, image analysis, and mRNA-seq. The central results showed that NLI was associated with long-term animal growth retardation, cardiomyocyte hyperpolyploidy, and extensive transcriptomic rearrangements. Many changes were known manifestations of heart pathologies, including DNA and telomere instability, inflammation, fibrosis, and reactivation of fetal gene programs. Bioinformatic analysis suggested these traits could stem from impaired thyroid hormone, calcium, and glutathione signaling. The study concludes that NLI-induced ploidy-related epigenetic alterations may permanently alter cardiomyocyte gene networks, providing evidence that NLI can be a trigger for developmental programming of adult cardiovascular disease. Limitations include the use of a rat model, with translational uncertainty to humans, and analysis limited to left ventricular cardiomyocytes.
