Gestational and lactational α-linolenic acid availability induces epigenetic changes in the brain of mouse offspring

Gestational and lactational α-linolenic acid availability induces epigenetic changes in the brain of mouse offspring Public Deposited

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He, Fuli
- Affiliation: Gillings School of Global Public Health, Department of Nutrition

Abstract

It has been acknowledged that dietary n-3 fatty acids improve memory and learning, in part by altering gene expression in the brain. However, the exact mechanisms are far from being clear, especially for α-linolenic acid (ALA). Inadequate perinatal nutrition can induce persistent changes in offspring phenotype, acting through epigenetic process. We investigated the effects of maternal ALA intakes on the epigenetic regulation of memory-associated genes, in the offspring brains, at the end of lactation (postnatal day 19, P19). Postnatal ALA supplementation altered mRNA expression of Mecp2, Ppp1cc, Reelin and Dnmt3a, while ALA deficiency during gestation induced changes in methylation of CpG sites in either promoter or intron1 of these genes. In addition, bivariate analysis indicated some significant associations between CpG site-specific methylation and the expression of Dnmt3a (p < 0.05). In summary, the interplay between ALA availability during gestation and lactation can differentially alter methylation and expression of genes involved in neurogenesis and synaptic plasticity, potentially affecting brain development and memory-related biological processes. However, further studies are needed to confirm the physiological effects of ALA.

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