Abstract
Maternal body mass index (BMI) and gestational weight gain (GWG) impacts both the mother's and the child's health, and epigenetic modifications have been suggested to mediate some of these effects in offspring. This systematic review aimed to summarize the current literature on associations between maternal BMI and GWG and epigenetic marks. We performed systematic searches in PubMed and EMBASE and manual searches of reference lists. We included 49 studies exploring the association between maternal BMI and/or GWG and DNA methylation or miRNA; 7 performed in maternal tissues, 13 in placental tissue and 38 in different offspring tissues. The most consistent findings were reported for the relationship between maternal BMI, in particular pre-pregnant BMI, and expression of miRNA Let-7d in both maternal blood and placental tissue, methylation of the gene HIF3A in umbilical cord blood and umbilical tissue, and with expression in the miR-210 target gene, BDNF in placental tissue and cord blood. Correspondingly, methylation of BDNF was also found in placental tissue and cord blood. The current evidence suggests that maternal BMI is associated with some epigenetic signatures in the mother, the placenta and her offspring, which could indicate that some of the effects proposed by the Developmental Origins of Health and Disease-hypothesis may be mediated by epigenetic marks. In conclusion, there is a need for large, well-designed studies and meta-analyses that can clarify the relationship between BMI, GWG and epigenetic changes.
Highlights
29 studies examined the association of epigenetic marks to maternal body mass index (BMI), two related to gestational weight gain (GWG), 15 to both maternal BMI and GWG, and one to maternal BMI and fat mass
Pre-pregnancy BMI was used in 37 of the included studies, while 12 used maternal BMI measured in pregnancy
This systematic review included 49 studies that examined the association of DNA methylation or miRNA to maternal BMI and/or GWG
Summary
Pre-pregnancy overweight and obesity are associated with increased risk of pregnancy complications, such as gestational diabetes mellitus,[1,2,3,4,5,6,7] preeclampsia,[1,2,8,9] macrosomia[2] and stillbirth.[8]Intrauterine exposure to high maternal adiposity or high gestational weight gain (GWG) is associated with adverse fetal development and may influence the offspring’s health later in life, according to the Developmental Origins of Health and Disease (DOHaD) hypothesis.[10,11,12,13] whether the observed effects are due to intrauterine effects directly following mother’s overweight or explained by shared environmental or genetic factors is under debate.[14]Environmental factors may translate into epigenetic modifications that can alter gene expression without changing the DNA-sequence, such as DNA methylation, histone modification or micro-RNAs (miRNAs).[15,16] DNA methylation results from the addition of a methyl group to the 5 0-C, modifying the interactions between DNA and proteins, for example, transcriptional machinery, and could change gene expression.[17]. Pre-pregnancy overweight and obesity are associated with increased risk of pregnancy complications, such as gestational diabetes mellitus,[1,2,3,4,5,6,7] preeclampsia,[1,2,8,9] macrosomia[2] and stillbirth.[8]. Intrauterine exposure to high maternal adiposity or high gestational weight gain (GWG) is associated with adverse fetal development and may influence the offspring’s health later in life, according to the Developmental Origins of Health and Disease (DOHaD) hypothesis.[10,11,12,13] whether the observed effects are due to intrauterine effects directly following mother’s overweight or explained by shared environmental or genetic factors is under debate.[14].
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