Maternal malnutrition during pregnancy can impact fetal neural development and alter brain performance of the offspring. Using a well-characterized maternal-protein-restriction-model in rat, we showed that the differentiation of neural stem cells was altered in fetal hypothalamus. A transcriptomic analysis revealed altered expression of several key genes involved in the regulation of mRNA stability/translation and histone modification. The Mettl14 gene, encoding a member of the m6A methyltransferase complex was underexpressed in the protein-restricted fetuses, while the Fto gene, encoding a m6A eraser, was overexpressed. This was associated with a global reduction of the m6A level in the fetal hypothalamus. In light of recent findings showing direct interactions between DNA epigenetic marks and m6A methylation complex activity, we re-explored our data and performed a global chromatin analysis by ATACseq. Using in-silico analysis of our transcriptomic and epigenetic data with publicly available lists of molecular targets of specific epigenetic and epitranscriptomic modifiers, we identified few genes that combine the following characteristics: (1) a lower expression in the protein-restricted fetal hypothalamus, (2) the presence of an ATACseq peak in their 3’UTR, consistent with the presence of specific histone modifications, (3) known as potential targets of the m6A methylation complex and harboring consensus motifs for this epitranscriptomic modification in their 3’UTR. Among these genes, Camsap1, Nrcam and Enc1 are involved in axonal cone growth through the control of cytoskeleton activity and therefore neural development and may represent good targets for nutritional regulation of fetal brain development. The exact mechanisms involved need to be further identified.