Genomic imprinting is a widespread epigenetic phenomenon in mammals and many imprinted genes are expressed in the developing hypothalamus and placenta. The placenta and brain are very different structures with very different roles, but in the pregnant mother they functionally interact coordinating and ensuring the provision of nutrients, timing of parturition and priming of hypothalamus for maternal care and nurturing. This interaction has been evolutionarily fine-tuned to optimise infant survival such that when resources are poor, the mother 'informs' this condition to the foetus producing a thrifty phenotype that is adapted to survive scarce resources after birth.
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DNA Imprinting and Differentially Expressed Genes in Muscle of Submitted to Early Weaning Management.
Epigenomes
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School of Veterinary and Animal Science (FMVZ), São Paulo State University (Unesp), Botucatu 18618-681, SP, Brazil.
Early weaning management followed by energy supplementation can lead to metabolic alterations in the calf that exert long-term effects on the animal's health and performance. It is believed that the main molecular basis underlying these metabolic adaptations are epigenetic mechanisms that regulate, activate, or silence genes at different stages of development and/or in response to different environmental stimuli. However, little is known about postnatal metabolic programming in .
View Article and Find Full Text PDFPaternal impact on the developmental programming of sexual dimorphism.
Front Cell Dev Biol
December 2024
Institute of Experimental Genetics, Helmholtz Munich GmbH, German Research Center for Environmental Health, Neuherberg, Germany.
Sexual dimorphism involves distinct anatomical, physiological, behavioral, and developmental differences between males and females of the same species, influenced by factors prior to conception and during early development. These sex-specific traits contribute to varied phenotypes and individual disease risks within and across generations and understanding them is essential in mammalian studies. Hormones, sex chromosomes, and imprinted genes drive this dimorphism, with over half of quantitative traits in wildtype mice showing sex-based variation.
View Article and Find Full Text PDFImpact of excess sugar on the whole genome DNA methylation pattern in human sperm.
Epigenomics
December 2024
Epigenetics and Diabetes Unit, Department of Clinical Sciences in Malmö, Lund University Diabetes Centre, Lund University, Scania University Hospital, Malmö, Sweden.
Aims, Patients & Methods: Dietary factors may regulate the epigenome. We aimed to explore whether a diet intervention, including excess sugar, affects the methylome in human sperm, and to describe the sperm methylome. We used Whole Genome Bisulfite Sequencing (WGBS) to analyze DNA methylation in sperm taken at three time points from 15 males during a diet intervention; i) at baseline, ii) after one week on a standardized diet, and iii) after an additional week on a high-sugar diet providing 150% of their estimated total energy expenditure.
View Article and Find Full Text PDFEnhancing HBV-specific T cell responses through a combination of epigenetic modulation and immune checkpoint inhibition.
Hepatology
December 2024
Department of Gastroenterology, Hepatology, Infectious Diseases and Endocrinology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
Objective: Chronic HBV infection (CHB) exhausts HBV-specific T cells, develops epigenetic imprints that impair immune responses, and limits the effectiveness of immune checkpoint inhibitor (ICI) monotherapy, such as αPD-L1. This study aimed to determine whether the DNA methyltransferase inhibitor decitabine (DAC) could reverse these epigenetic imprints and enhance ICI efficacy in restoring HBV-specific T cell responses.
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The expanding landscape of genetic causes of obesity.
Pediatr Res
December 2024
Division of Molecular Genetics, Department of Pediatrics, Columbia University Irving Medical Center, New York, NY, USA.
Obesity and weight regulation disorders are determined by the combined effects of genetics and environment. Polygenic obesity results from the combination of common variants in several genes which predisposes the individual to obesity and its related complications. In contrast, monogenic obesity results from changes in single genes, especially those in leptin-melanocortin pathway, and presents with early onset severe obesity, with or without other syndromic features.
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