ReviewHistochemistry and cell biology2026
Effects of obesity on DNA methylation and DNA methyltransferases in the reproductive system.
Review in Histochemistry and cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity is increasingly recognized as a condition with profound systemic and epigenetic consequences. However, the molecular mechanisms linking obesity to reproductive dysfunction remain incompletely understood. Accumulating evidence suggests that epigenetic regulation, particularly DNA methylation, contributes to and is modified by obesity, thereby influencing gene expression in gonadal tissues and germ cells. DNA methylation is essential for normal oogenesis and spermatogenesis and is mediated by DNA methyltransferases (DNMTs), whose expression and activity are tightly regulated throughout germ cell development. This review synthesizes current experimental and clinical evidence regarding obesity-associated alterations in DNMT expression and DNA methylation patterns across female and male reproductive systems and examines how these epigenetic disruptions contribute to infertility. Obesity is most frequently associated with a hypermethylated epigenetic landscape in female reproductive tissues, whereas the male germline more commonly exhibits global or locus-specific hypomethylation, reflecting sex-specific epigenetic responses to metabolic stress. Studies spanning ovarian tissue, oocytes, sperm, and early embryos demonstrate that obesity-induced DNMT dysregulation and DNA methylation remodeling disrupt transcriptional programs governing folliculogenesis, spermatogenesis, and embryo development.
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