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Maternal type 1 diabetes might protect offspring through epigenetic modifications

Nature Metabolism volume 7, pages 2197–2198 (2025)Cite this article

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Children born to mothers with type 1 diabetes (T1D) are less likely to develop T1D than those with an affected father or sibling. We identified modifications of DNA methylation at multiple T1D risk genes in blood samples from children exposed to maternal T1D. These changes were linked to decreased islet autoimmunity risk.

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Fig. 1: Maternal T1D methylation propensity score associates with islet autoimmunity in children not exposed to maternal T1D.

References

  1. Lernmark, A. et al. Looking back at the TEDDY study: lessons and future directions. Nat. Rev. Endocrinol. 21, 154–165 (2025). This Review summarizes key findings on environmental factors associated with risk or protection against islet autoimmunity.

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  2. Warram, J. H., Krolewski, A. S., Gottlieb, M. S. & Kahn, C. R. Differences in risk of insulin-dependent diabetes in offspring of diabetic mothers and diabetic fathers. N. Engl. J. Med. 311, 149–152 (1984). This paper reports the lower risk of T1D in offspring of mothers with T1D.

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  4. Bonifacio, E. et al. Maternal type 1 diabetes reduces the risk of islet autoantibodies: relationships with birthweight and maternal HbA1c. Diabetologia 51, 1245–1252 (2008). This paper reports the reduced risk of islet autoimmunity in offspring of mothers with T1D and discusses potential mechanisms.

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  5. Klibaner-Schiff, E. et al. Environmental exposures influence multigenerational epigenetic transmission. Clin. Epigenetics 16, 145 (2024). A review article that presents current understanding of how environmental exposures influence the epigenome.

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This is a summary of: Ott, R. et al. Blood methylome signatures in children exposed to maternal type 1 diabetes are linked to protection against islet autoimmunity. Nat. Metab. https://doi.org/10.1038/s42255-025-01403-w (2025).

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Maternal type 1 diabetes might protect offspring through epigenetic modifications. Nat Metab 7, 2197–2198 (2025). https://doi.org/10.1038/s42255-025-01406-7

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