Maternal obesity alters histone modifications mediated by the interaction between EZH2 and AMPK, impairing neural differentiation in the developing embryonic brain cortex.

ABSTRACT: Neurodevelopmental disorders have complex origins that manifest early during embryonic growth and are associated with intricate gene regulation dynamics. A perturbed metabolic environment such as hyperglycemia or dyslipidemia, particularly due to maternal obesity, poses a threat to the optimal development of the embryonic central nervous system. Accumulating evidence suggests that these metabolic irregularities during pregnancy may alter neurogenesis pathways, thereby predisposing the developing fetus to neurodevelopmental disorders. One primary mechanism through which such disruptions may occur involves changes in histone modifications resulting from fluctuations in the expression of histone-modifying enzymes or the availability of their substrates. Herein, we have used a rat model of mat

SUBMITTER: Alawathugoda TT 

PROVIDER: S-EPMC11847741 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature