Parental lifestyle patterns around pregnancy and risk of childhood obesity in four European birth cohort studies

Lecorguillé, Marion; Schipper, Mireille; O’Donnell, Aisling T.; Aubert, Adrien M.; Tafflet, Muriel; Gassama, Malamine; Douglass, Alexander S.; Hébert, James R.; Kelleher, Cecily; Munier, Charles; Phillips, Catherine M.; Gaillard, Romy; Lioret, Sandrine; Heude, Barbara

doi:10.1016/s2214-109x(23)00090-6

Cited by 6 publications

(5 citation statements)

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Section: Discussionmentioning

confidence: 99%

“…Recent studies have found that some diseases in the offspring are closely related to parents' lifestyle (including obesity), and underlying mechanism employs a variety of epigenetics regulations, such as DNA methylation, histone modification, sperm small noncoding RNA, and long noncoding RNA (Baker & Friedman, 2018; Fleming et al, 2018; Godfrey et al, 2017; Lecorguillé et al, 2023; Xu, Hong, et al, 2021). By knocking out Ezh1/2 in oocytes, we found that mitochondria were damaged in oocytes and subsequent early embryonic development, resulting in abnormal material and energy metabolism, autophagy, and apoptosis in embryonic cells.…”

Section: Discussionmentioning

confidence: 99%

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Maternal Ezh1/2 deficiency impairs the function of mitochondria in mouse oocytes and early embryos

Zhang,

Deng,

Jiang

et al. 2024

Journal Cellular Physiology

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Maternal histone methyltransferase is critical for epigenetic regulation and development of mammalian embryos by regulating histone and DNA modifications. Here, we reported a novel mechanism by revealing the critical effects of maternal Ezh1/2 deletion on mitochondria in MII oocytes and early embryos in mice. We found that Ezh1/2 knockout in mouse MII oocytes impaired the structure of mitochondria and decreased its number, but membrane potential and respiratory function of mitochondrion were increased. The similar effects of Ezh1/2 deletion have been observed in 2‐cell and morula embryos, indicating that the effects of maternal Ezh1/2 deficiency on mitochondrion extend to early embryos. However, the loss of maternal Ezh1/2 resulted in a severe defect of morula: the number, membrane potential, respiratory function, and ATP production of mitochondrion dropped significantly. Content of reactive oxygen species was raised in both MII oocytes and early embryos, suggesting maternal Ezh1/2 knockout induced oxidative stress. In addition, maternal Ezh1/2 ablation interfered the autophagy in morula and blastocyst embryos. Finally, maternal Ezh1/2 deletion led to cell apoptosis in blastocyst embryos in mice. By analyzing the gene expression profile, we revealed that maternal Ezh1/2 knockout affected the expression of mitochondrial related genes in MII oocytes and early embryos. The chromatin immunoprecipitation‐polymerase chain reaction assay demonstrated that Ezh1/2 directly regulated the expression of genes Fxyd6, Adpgk, Aurkb, Zfp521, Ehd3, Sgms2, Pygl, Slc1a1, and Chst12 by H3K27me3 modification. In conclusion, our study revealed the critical effect of maternal Ezh1/2 on the structure and function of mitochondria in oocytes and early embryos, and suggested a novel mechanism underlying maternal epigenetic regulation on early embryonic development through the modulation of mitochondrial status.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Maternal Ezh1/2 deficiency impairs the function of mitochondria in mouse oocytes and early embryos

Zhang,

Deng,

Jiang

et al. 2024

Journal Cellular Physiology

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“…Pollutants act as endocrinological disruptors, with a positive association being observed between maternal exposure and concentrations of adipokines, adiponectin, and leptin in the umbilical cord of newborns. 7 , 8 …”

Section: Prenatal Periodmentioning

confidence: 99%

What causes obesity in children and adolescents?

Nogueira-de-Almeida,

Weffort,

Ued

et al. 2024

Jornal de Pediatria

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“…Parental smoking frequency 1-3, 5-8 Coded as: 1 for does not smoke at all; 2 for <1/day; and 3 for �1/day. Parental smoking has been associated with an increased risk of childhood obesity and overweight in some studies [32].…”

Section: Parental Weekly Incomementioning

confidence: 99%

Impact of prenatal maternal dietary exclusion on childhood obesity and overweight risk

Horne,

Kabir,

Alam

2024

PLoS ONE

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Background Child birthweight is a measure of fetal nutrition that is primarily determined by prenatal maternal (PM) diet. Child birthweight and child obesity/overweight risk are well established to be linked. Nevertheless, no studies have investigated the impact of PM dietary exclusion on child obesity/overweight risk or body mass index z-score (BMIz). Objectives The study aimed to determine whether PM dietary exclusion affected the child’s BMIz, obesity/overweight risk, whether child birthweight serves as a mediator of this, and whether PM use of dietary supplements can protect against this. Methods Waves within the years 2004–2019 from the Longitudinal Study of Australian Children, a population-based cohort study, were analyzed. The participants were aged 0 to 15 years during these waves of the study. Analysis was conducted using logistic and linear models. A total of 5,107 participants were involved in the first wave of the study. Results The PM exclusion of fish was associated with a higher risk of being underweight at age 14 or 15 years and mild-to-moderate obesity at age 6 or 7 years. The PM exclusion of egg was associated with a higher risk of being overweight at age 14 or 15 years. The exclusion of dairy was associated with more mixed effects. Mediation effects did not reach statistical significance. Moderation effects involving PM dietary supplement use, when they did occur, were associated with higher child BMIz and usually a higher risk of obesity/overweight. Conclusions Fish and eggs are likely important parts of PM diets for preventing childhood obesity and overweight. Further studies will be needed to determine reasons for this and the apparent adverse effects of dietary supplements on overweight/obesity risk.

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Parental lifestyle patterns around pregnancy and risk of childhood obesity in four European birth cohort studies

Cited by 6 publications

References 0 publications

Maternal Ezh1/2 deficiency impairs the function of mitochondria in mouse oocytes and early embryos

Maternal Ezh1/2 deficiency impairs the function of mitochondria in mouse oocytes and early embryos

What causes obesity in children and adolescents?

Impact of prenatal maternal dietary exclusion on childhood obesity and overweight risk

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