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

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• 作者：Zhao-Jia Ge (1) (2) (3)
  Qiu-Xia Liang (2)
  Yi Hou (2)
  Zhi-Ming Han (2)
  Heide Schatten (4)
  Qing-Yuan Sun (2)
  Cui-Lian Zhang (1) (3)
  
  1. Reproductive Medicine Center ; Henan Provincial People鈥檚 Hospital ; Zhengzhou ; 450003 ; Henan Province ; P.R. China
  2. State Key Laboratory of Reproductive Biology ; Institute of Zoology ; Chinese Academy of Sciences ; Beijing ; 100101 ; P.R. China
  3. Reproductive Medicine Center ; People鈥檚 Hospital of Zhengzhou University ; Zhengzhou ; 450003 ; Henan province ; P.R. China
  4. Department of Veterinary Pathobiology ; University of Missouri ; 65211 ; Columbia ; MO ; USA
  
• 关键词：Spermotozoa ; Offspring ; Methylation ; Maternal diabetes/obesity
• 刊名：Reproductive Biology and Endocrinology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：12
• 期：1
• 全文大小：820 KB
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• 刊物主题：Reproductive Medicine; Endocrinology;
• 出版者：BioMed Central
• ISSN：1477-7827

文摘

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.