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Life sciences · Journal article
American Journal of Physiology-heart and Circulatory Physiology · September 8, 2026
Raises a question worth testing. It does not answer one.
This preclinical mouse study demonstrates that maternal high-fat diet induces sex-dependent epigenetic and transcriptomic changes in offspring hearts that persist to adulthood, with male offspring showing pathological remodeling signatures and females showing adaptive responses. The work identifies potential developmental mechanisms but requires human validation and does not yet support clinical intervention.
Experimental animal model study with maternal diet intervention and sex stratification. Mouse offspring exposed in utero to maternal high-fat diet (Off-HFD) or maternal regular diet (Off-RD); stratified by sex.. Intervention: Maternal high-fat diet during pregnancy. Compared with: Maternal regular diet.
Offspring of HFD-fed mothers (Off-HFD) exhibit obesity, dyslipidemia, and metabolic inflexibility compared with offspring of regular diet–fed mothers (Off-RD) Male Off-HFD mice developed more severe cardiac phenotype with hypertension, increased vascular stiffness, cardiac dysfunction, and fibrosis; both sexes showed progressive cardiac hypertrophy DNA methylation analysis revealed extensive, sex-dependent alterations in genes involved in cardiac development, lipid metabolism, hypertrophic growth, and inflammatory signaling
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Findings suggest maternal obesity triggers early epigenetic programming that predisposes offspring to later cardiovascular disease, particularly males. However, this is a mechanistic animal study; human epidemiological or intervention studies are needed to determine if targeting these epigenetic pathways can reduce cardiovascular risk in human offspring.
Mechanistic mouse model study identifying epigenetic and transcriptomic associations with maternal obesity and cardiac remodeling, but without functional validation or human translation to support clinical application.
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Findings suggest maternal obesity triggers early epigenetic programming that predisposes offspring to later cardiovascular disease, particularly males. However, this is a mechanistic animal study; human epidemiological or intervention studies are needed to determine if targeting these epigenetic pathways can reduce cardiovascular risk in human offspring.
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Maternal o besity during pregnancy predisposes the offspring to a high risk of developing cardiovascular and metabolic diseases later in life. This study investigated cardiac perturbations caused by maternal obesity by utilizing a mouse model of maternal high-fat diet (HFD)–induced obesity that recapitulates metabolic abnormalities observed in humans. Our study revealed that offspring of HFD-fed mothers (Off-HFD) exhibit a progression of obesity, dyslipidemia, and metabolic inflexibility when compared with offspring of regular diet–fed mothers (Off-RD). Deeper investigation of cardiac function revealed profound functional, metabolic, vascular, and immune perturbations in adult Off-HFD mice, with marked sex-specific differences. Although both male and female Off-HFD mice developed progressive cardiac hypertrophy, male offspring exhibited a more severe phenotype characterized by hypertension, increased vascular stiffness, cardiac dysfunction, and fibrosis. To identify potential mechanisms underlying these changes, we performed DNA methylation analysis in collected hearts of newly weaned and adult offspring. This analysis revealed extensive, sex-dependent alterations in DNA methylation within or nearby genes involved in cardiac development, lipid metabolism, hypertrophic growth, and inflammatory signaling. Importantly, many of these epigenetic alterations persisted into adulthood, suggesting that maternal obesity establishes a durable molecular memory in the offspring heart. Consistent with these findings, transcriptome analysis of adult hearts revealed activation of gene programs associated with heart failure and pathological cardiac remodeling in male Off-HFD mice, whereas female Off-HFD mice showed activation of pathways consistent with adaptive or cardioprotective responses. Together, these findings demonstrate that maternal HFD induces early-life epigenetic remodeling in the offspring heart that persists into adulthood and is associated with sex-specific metabolic, functional, vascular, and immune dysregulations. By linking early epigenomic changes to adult cardiac disease susceptibility, this study identifies potential developmental windows for preventive and early therapeutic interventions aimed at reducing cardiovascular risk in offspring exposed to maternal obesity in utero.
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