ArticleNature communications2024
Multigenerational paternal obesity enhances the susceptibility to male subfertility in offspring via Wt1 N6-methyladenosine modification.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Dietary Patterns Modulate Ozone-Induced Reproductive Injury in C57BL/6J Mice.Environment & health (Washington, D.C.) · 2026Article
- N6-Methyladenosine and 5-Methylcytosine Epitranscriptomic Regulation of Male Reproduction and Fertility.Biology · 2026Review
- Review
- Bridging maternal effects and epitranscriptomics: A novel perspective in developmental biology.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Review
- The role of m6A modification in spermatogenic dysfunction.Molecular biology reports · 2026Review
- Brain neuronal CG9593/ANGPTL4 activation mediates paternally acquired motor disorders.Science advances · 2026Article
- Prenatal cadmium exposure and male infertility in mice: A multi-generational mechanistic study.Eco-Environment & Health · 2026Article
- Epididymal macrophage senescence contributes to sperm motility decrease upon environmental stress.Science advances · 2026Article
- Research progress on m6A RNA methylation modification in human reproduction related diseases.European journal of medical research · 2025Review
- Obesity in reproduction: Mechanisms from fertilization to post‑uterine development (Review).International journal of molecular medicine · 2025Review
- Effect of lycium barbarum polysaccharide on ameliorating high-fat diet-damaged spermatogenesis via PCSK9 and TLR4 signaling pathways in obese mice.Molecular biology reports · 2025Article
- Beyond Genes: Mechanistic and Epidemiological Insights into Paternal Environmental Influence on Offspring Health.Current environmental health reports · 2025Review
- Emerging Orchestrator of Ecological Adaptation: mMolecular ecology · 2025Review
- Epitranscriptomic Role of m6A in Obesity-Associated Disorders and Cancer Metabolic Reprogramming.Genes · 2025Review
- The impact, mechanisms and prevention strategies of environmental endocrine disruptors on male reproductive health.Frontiers in endocrinology · 2025Review
- Potential role of 4-hydroxyisoleucine in enhancing fertility in male mice with diet-induced obesity.Frontiers in endocrinology · 2025Article
- Association between the age-adjusted visceral adiposity index (AVAI) and female infertility status: a cross-sectional analysis of the NHANES 2013-2018.Lipids in health and disease · 2024Article
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
There is strong evidence that obesity is a risk factor for poor semen quality. However, the effects of multigenerational paternal obesity on the susceptibility to cadmium (a reproductive toxicant)-induced spermatogenesis disorders in offspring remain unknown. Here, we show that, in mice, spermatogenesis and retinoic acid levels become progressively lower as the number of generations exposed to a high-fat diet increase. Furthermore, exposing several generations of mice to a high fat diet results in a decrease in the expression of Wt1, a transcription factor upstream of the enzymes that synthesize retinoic acid. These effects can be rescued by injecting adeno-associated virus 9-Wt1 into the mouse testes of the offspring. Additionally, multigenerational paternal high-fat diet progressively increases METTL3 and Wt1 N6-methyladenosine levels in the testes of offspring mice. Mechanistically, treating the fathers with STM2457, a METTL3 inhibitor, restores obesity-reduced sperm count, and decreases Wt1 N6-methyladenosine level in the mouse testes of the offspring. A case-controlled study shows that human donors who are overweight or obese exhibit elevated N6-methyladenosine levels in sperm and decreased sperm concentration. Collectively, these results indicate that multigenerational paternal obesity enhances the susceptibility of the offspring to spermatogenesis disorders by increasing METTL3-mediated Wt1 N6-methyladenosine modification.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.