Epigenetic Modulation of Fetal Growth and Brain Development: Effects of Dietary Factors and Pollutants

Dear Colleagues,

Epigenetic stability of the genome ensures tissue-specific gene expression in an organism. It also encodes fingerprints for the development of adult diseases. Early-life development is not static anymore as growing pollutant exposure and nutritional imbalance transform its permeability and plasticity. Environmental epigenetics reflects a dynamic relationship between plasticity and disease risks. It deals with factors that interact with the fetus those shape expression profiles of genes across the life, characterizes fetal vulnerability for its growth & development, and modulates life-long disease risks. Epigenetic modifications via DNA methylation, microRNA expression, and histone modification can control phenotypic programming of neonatal adiposity and endocrine-metabolic disorders in their adult life. An imbalance in dietary fats in utero can induce a stable epigenetic change that may affect fetal programming of hypothalamic inflammation, resulting in altered energy expenditure, brain signalling, endocrine response, and metabolic alteration in the progeny. On the other hand, maternal high-fat promotes low-grade inflammation during intrauterine development, profoundly changes maternal metabolic state, placental changes in the expression of a microRNA-mRNA-gene network, and modulates intrauterine inflammation, fetal growth, glucose, and lipid metabolism in their adult life.

Fetal brain development is characterized by a coordinated change in gene expression by interacting transcription factors and epigenetic processes. The biological importance of DNA methylation as a significant epigenetic carrier in modulating phenotype and gene expression is scrutinized extensively. While cytosine methylation of genes lowers its expression, the hydroxymethylcytosine promotes higher gene expression. The presence of 5hmC in the regulatory region of the genome in human and rodent fetal brains, in neuronal maturation, and synaptogenesis suspects that abnormal regulation of hydroxymethylcytosine enrichment in genes could contribute to neurodevelopment disorders. Whether early-life exposure to pollutants or dietary imbalance modulates fetal growth and brain development through these epigenetic modifications is unknown.

The special issue aims to highlight the impact of epigenetic modification on fetal growth and brain development and its risk of developing metabolic and endocrine disorders. The major aim is to collate high-quality clinical and pre-clinical data covering these research domains. Therefore, authors are invited to submit original research articles or comprehensive reviews on epigenetic and metabolic risks in developing adult disease due to early early-life exposure to dietary factors and pollutants.

Dr. Sanjay Basak
Prof. Dr. Asim K. Duttaroy
Guest Editors

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• epigenetics and brain signalling
• hypothalamic inflammation
• hydroxymethylation and brain development
• pollutants and fetal development
• fetal growth & adiposity
• insulin and leptin signalling
• endocrine disruption and epigenetics
• dietary fats imbalance
• intrauterine inflammation and adiposity
• epigenomic modulation and metabolism
• endocrine-metabolic nexus