母体肥胖和糖尿病可能导致小鼠后代精子中的DNA甲基化改变。
Maternal obesity and diabetes may cause DNA methylation alteration in the spermatozoa of offspring in mice.
作者信息
Ge Zhao-Jia, Liang Qiu-Xia, Hou Yi, Han Zhi-Ming, Schatten Heide, Sun Qing-Yuan, Zhang Cui-Lian
机构信息
Reproductive Medicine Center, Henan Provincial People's Hospital, Zhengzhou 450003, Henan Province, P,R, China.
出版信息
Reprod Biol Endocrinol. 2014 Apr 11;12:29. doi: 10.1186/1477-7827-12-29.
BACKGROUND
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.
METHODS
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.
RESULTS
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.
CONCLUSIONS
These results indicate that pre-gestational diabetes and/or obesity can alter DNA methylation in offspring spermatozoa.
背景
糖尿病和/或肥胖母亲对后代的不良影响可能会传递给下一代。然而，其背后的机制仍不清楚。表观遗传学可能在此过程中起关键作用。
方法
为了证实这一假设，我们利用链脲佐菌素（STZ）和高脂饮食（HFD）诱导的小鼠模型，研究了糖尿病和/或肥胖母亲后代精子中几个印记基因的DNA甲基化情况。
结果
我们发现，与正常母亲后代的精子相比，肥胖母亲后代的精子中Peg3的DNA甲基化显著增加。糖尿病母亲后代的精子中H19的DNA甲基化明显高于非糖尿病母亲后代的精子。
结论
这些结果表明，孕前糖尿病和/或肥胖会改变后代精子中的DNA甲基化。
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