ArticleeLife2024
Maternal obesity may disrupt offspring metabolism by inducing oocyte genome hyper-methylation via increased DNMTs.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Metabolic regulation of oocyte maturation and early embryo development in mammals.Life metabolism · 2026Review
- Maternal obesity imprints methylation marks in oocytes to drive intergenerational metabolic dysfunction.Nature metabolism · 2026Article
- Cross-species metabolic profiling of follicular compartments in obesity.Life medicine · 2026Article
- A review of the association between abnormal body mass index and oocyte quality.Journal of ovarian research · 2026Review
- Ovarian aging: maintenance and activation of the primordial follicle pool.Journal of ovarian research · 2026Review
- Epigenetic deciphering of ovarian aging: multilayer interactive mechanisms and targeted reversal strategies.Epigenetics & chromatin · 2026Review
- Effects of obesity on DNA methylation and DNA methyltransferases in the reproductive system.Histochemistry and cell biology · 2026Review
- Cross-Generational Integration of Exercise and Nutritional Encoding in Offspring Adipose Genomics.International journal of molecular sciences · 2026Review
- From Risks to Roots: The Multifactorial Etiopathogenesis of Childhood Obesity.International journal of molecular sciences · 2026Review
- Grandmaternal Obesity and Risks of Birth Asphyxia-Related Complications in Grand-Offspring: A Countrywide Three-Generation Study.Obesity (Silver Spring, Md.) · 2025Article
- Mechanism of crosstalk between DNA methylation and histone acetylation and related advances in diagnosis and treatment of premature ovarian failure.Epigenetics · 2025Review
- Article
- Dynamic Rendition of Adipose Genes Under Epigenetic Regulation: Revealing New Mechanisms of Obesity Occurrence.Current issues in molecular biology · 2025Review
- Prenatal melatonin reprograms liver injury in male pups caused by maternal exposure to a high-fat diet and microplastics.Apoptosis : an international journal on programmed cell death · 2025Article
- Maternal Nutrition, Toxicants, and Epigenetic Programming of Obesity Across Generations.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- The dual burden of obesity: decoding metabolism and female reproductive endocrinology.Frontiers in physiology · 2025Review
- EVA1A Regulates Hepatic Lipid Homeostasis by Modulating CD36 Expression and Its Palmitoylation.Research (Washington, D.C.) · 2025Article
- Childhood obesity from the genes to the epigenome.Frontiers in endocrinology · 2024Review
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Authors and funding
15 authors.
Funding
Abstract
Maternal obesity has deleterious effects on the process of establishing oocyte DNA methylation; yet the underlying mechanisms remain unclear. Here, we found that maternal obesity disrupted the genomic methylation of oocytes using a high-fat diet (HFD) induced mouse model, at least a part of which was transmitted to the F2 oocytes and livers via females. We further examined the metabolome of serum and found that the serum concentration of melatonin was reduced. Exogenous melatonin treatment significantly reduced the hyper-methylation of HFD oocytes, and the increased expression of DNMT3a and DNMT1 in HFD oocytes was also decreased. These suggest that melatonin may play a key role in the disrupted genomic methylation in the oocytes of obese mice. To address how melatonin regulates the expression of DNMTs, the function of melatonin was inhibited or activated upon oocytes. Results revealed that melatonin may regulate the expression of DNMTs via the cAMP/PKA/CREB pathway. These results suggest that maternal obesity induces genomic methylation alterations in oocytes, which can be partly transmitted to F2 in females, and that melatonin is involved in regulating the hyper-methylation of HFD oocytes by increasing the expression of DNMTs via the cAMP/PKA/CREB pathway.
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