Abstract
Unfavorable maternal diet during pregnancy can predispose the offspring to diseases later in life, such as hypertension, metabolic syndrome, and obesity. However, the molecular basis for this phenomenon of “developmental programming” is poorly understood. We have recently shown that a diet nutritionally optimized for pregnancy can nevertheless be harmful in the context of diabetic pregnancy in the mouse, associated with a high incidence of neural tube defects and intrauterine growth restriction. We hypothesized that placental abnormalities may contribute to impaired fetal growth in these pregnancies, and therefore investigated the role of maternal diet in the placenta. LabDiet 5015 diet was associated with reduced placental growth, commencing at midgestation, when compared to pregnancies in which the diabetic dam was fed LabDiet 5001 maintenance chow. Furthermore, by quantitative RT-PCR we identify 34 genes whose expression in placenta at midgestation is modulated by diet, diabetes, or both, establishing biomarkers for gene-environment interactions in the placenta. These results implicate maternal diet as an important factor in pregnancy complications and suggest that the early phases of placenta development could be a critical time window for developmental origins of adult disease.
Highlights
Maternal diet has long been known to be a key determinant for pregnancy success
Using a mouse model of diabetic pregnancy, we have recently shown that a diet nutritionally optimized for pregnancy can be harmful [9]
The diets differed in some other micronutrient components, these results are consistent with the notion that macronutrient composition of the maternal diet modulates the extent of intrauterine growth restriction in diabetic pregnancies
Summary
Maternal diet has long been known to be a key determinant for pregnancy success. Both undernutrition and malnutrition are harmful to development of the conceptus, increasing risk for spontaneous abortions, congenital malformations, and intrauterine growth restriction [1,2]. Unfavorable maternal diet, as reflected in abnormal birth weight, is believed to predispose the offspring to diseases later in life, such as hypertension, metabolic syndrome, and obesity [7,8]. In the context of maternal hyperglycemia, this diet interacts with maternal metabolic conditions, leading to a more than three-fold increased rate of neural tube defects compared to occurrence of these defects when the pregnant diabetic dam is fed a maintenance chow [9]. Under these adverse conditions even embryos that were not obviously malformed were negatively affected, as demonstrated by reduced fetal growth. The impaired fetal growth clearly suggested that nutrient supply to the fetus was impaired, and that the placenta, the major conduit of nutrients to the fetus, might be compromised
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