Paternal transgenerational glucose intolerance with epigenetic alterations in second generation offspring of GDM.
Paternal transgenerational glucose intolerance with epigenetic alterations in second generation offspring of GDM.
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DOI：
10.1038/aja.2013.72
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发表时间：
2013-06
影响因子：
2.9
通讯作者：
G. Ding;He-feng Huang
中科院分区：
文献类型：
--
作者：
G. Ding;He-feng Huang
Gestational diabetes mellitus (GDM) has been shown to be associated with high risk of diabetes in offspring. In addition to intergenerational transmission (F1 offspring), intrauterine hyperglycemia also has effects on the second generation (F2 offspring). However, the mechanisms involved and the possibilities of transgenerational transmission are still unclear. In a recent study published in Diabetes, we have utilized GDM mouse model to identify hyperglycemic intrauterine environment causing a high risk of diabetes in offspring by altering epigenetic modification. Furthermore, the results indicate that the abnormality of phenotype and imprinted genes expression are more obvious in male offspring than that of female. The changes of epigenetics in sperm may contribute to transgenerational transmission.A growing body of research suggests that exposure to the abnormal environment in uterus can lead to chronic health problems later in life. 1 Intrauterine hyperglycemia is a major characteristic of GDM and has been suggested as an important determinative factor for the risk of diabetes in adulthood, in addition to the effects of genetic factors. 2 The mechanism involved in the association between intrauterine hyperglycemia and a high risk of diabetes in offspring remains unclear. 3 In mammals, epigenetic reprogramming is involved in germ cells and early embryonic development. 4, 5 Because erasure and establishment of the genomic imprints for some imprinted genes begin when migratory primordial germ cells enter the embryonic genital ridge through gametogenesis, epigenetic abnormalities that occur during
