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01.12.2014 | Research | Ausgabe 1/2014 Open Access

Reproductive Biology and Endocrinology 1/2014

Maternal obesity and diabetes may cause DNA methylation alteration in the spermatozoa of offspring in mice

Reproductive Biology and Endocrinology > Ausgabe 1/2014
Zhao-Jia Ge, Qiu-Xia Liang, Yi Hou, Zhi-Ming Han, Heide Schatten, Qing-Yuan Sun, Cui-Lian Zhang
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1477-7827-12-29) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interest.

Authors’ contributions

GZJ, ZCL, HS and SQY designed and wrote the manuscript. LQX, HY and GZJ acquired data. HZM analyzed the data. All authors read and approved the final manuscript.



The adverse effects on offspring of diabetic and/or obese mothers can be passed to the next generation. However, the mechanisms behind this are still unclear. Epigenetics may play a key role during this process.


To confirm the hypothesis, we investigated the DNA methylation of several imprinted genes in spermatozoa of offspring from diabetic and/or obese mothers utilizing streptozotocin (STZ)- and high-fat-diet (HFD)-induced mouse models.


We found that the DNA methylation of Peg3 was significantly increased in spermatozoa of offspring of obese mothers compared to that in spermatozoa of offspring of normal mothers. The DNA methylation of H19 was significantly higher in spermatozoa of offspring of diabetic mothers than that in spermatozoa of offspring of non-diabetic mothers.


These results indicate that pre-gestational diabetes and/or obesity can alter DNA methylation in offspring spermatozoa.
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