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Diet-induced obesity affects miRNA expression in plasma extracellular vesicles of pregnant mice

ABSTRACT: Obesity during pregnancy is linked to a high risk of offspring overweight, insulin resistance, type 2 diabetes, and cardiometabolic disease in later life. However, the underlying mechanisms by which maternal factors drive these long-lasting effects remain to be fully elucidated. In our study, we have demonstrated that in diet-induced-obesity (DIO) pregnant mice, maternal small extracellular vesicles (sEV) in circulating system have the ability to cross the placental barrier and reach the liver of fetal mice, exerting a sustained adverse impact on offspring insulin sensitivity. Further investigations have revealed that pathogenically increased miR-29a-3p in maternal sEV from DIO mice can be delivered into livers of fetal offspring. Elevated miR-29a-3p subsequently alter epigenetic state in fetal liver via targeting several key methyltransferases and demethylases, interrupting the DNA methylation landscape, including hypomethylation of PGC-1α. Such epigenetic remodeling abnormally promotes early hepatic gluconeogenesis at fetal stage that contribute to the adult metabolic disturbance in offspring. Taken together, our finding suggests that the transplacental delivery of maternal sEV could serve as a potential mechanism for prenatal programming of metabolic health in offspring.

ORGANISM(S): Mus musculus

PROVIDER: GSE297729 | GEO | 2026/07/31

REPOSITORIES: GEO

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Diet-induced obesity affects miRNAs expression in fetal mouse liver

Project description:Obesity during pregnancy is linked to a high risk of offspring overweight, insulin resistance, type 2 diabetes, and cardiometabolic disease in later life. However, the underlying mechanisms by which maternal factors drive these long-lasting effects remain to be fully elucidated. In our study, we have demonstrated that in diet-induced-obesity (DIO) pregnant mice, maternal small extracellular vesicles (sEV) in circulating system have the ability to cross the placental barrier and reach the liver of fetal mice, exerting a sustained adverse impact on offspring insulin sensitivity. Further investigations have revealed that pathogenically increased miR-29a-3p in maternal sEV from DIO mice can be delivered into livers of fetal offspring. Elevated miR-29a-3p subsequently alter epigenetic state in fetal liver via targeting several key methyltransferases and demethylases, interrupting the DNA methylation landscape, including hypomethylation of PGC-1α. Such epigenetic remodeling abnormally promotes early hepatic gluconeogenesis at fetal stage that contribute to the adult metabolic disturbance in offspring. Taken together, our finding suggests that the transplacental delivery of maternal sEV could serve as a potential mechanism for prenatal programming of metabolic health in offspring.

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miR-29a-3p affects DNA methylation level in fetal mouse liver

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Investigation of placental DNA methylation in obese women exposed to Metformin during pregnancy

Project description:Maternal obesity in pregnancy is associated with increased birth-weight, obesity and premature mortality in adult offspring. The Effect of Metformin on Maternal and Fetal Outcomes in Pregnant Obese Women (EMPOWaR) trial was a randomised, double-blind, placebo-controlled trial carried out to determine whether exposure to Metformin would affect the offspring birth-weight centile. Obese women exposed to Metformin had increased insulin sensitivity at 36 weeks of pregnancy, but there were no differences in offspring birthweight. We obtained the placentas from these women to determine whether there were differences in DNA methylation of genes regulating fetal growth and metabolism. In a related study we investigated the gene expression in the same samples.

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Hofbauer cells and fetal brain microglia share transcriptional profiles and responses to maternal diet-induced obesity

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