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Placental weight was significantly reduced in the MNR pregnancies. Apart from a trend for fetal heart weight to be decreased (P http://en.wikipedia.org/wiki/Diglyceride MNR significantly increased both the area stained for PEPCK1, which increased 670%, and the density of staining, which increased by 250%, in the fetal liver (Figs 1 and 2). The effect of MNR did not differ with fetal sex (data not shown). As result of exposure to reduced nutrition the level of PEPCK1 in MNR http://www.selleckchem.com/products/GDC-0941.html fetuses had risen to approximately 63% of adult levels and was not significantly lower than in the pregnant adult. Figure 3A shows that mRNA for PCK1 was increased in the livers of fetuses of the mothers receiving reduced nutrition (2.3-fold; P http://www.selleckchem.com/products/AZD0530.html significant loss of DNA methylation in fetal livers of MNR mothers compared with CTR livers (Fig. 4). The moderate degree of maternal nutrient reduction imposed on the pregnant baboons and their fetuses in this study had only minor effects on overall fetal growth or growth of specific fetal organs (Nijland et al. 2007). Despite these limited effects on external phenotype, we have reported marked effects on detailed structure and gene and protein abundance in the placenta, fetal liver and kidney (Cox et al. 2006; Li et al. 2007; Nijland et al. 2007; Schlabritz-Loutsevitch et al. 2007). Similar studies of maternal nutrient reduction in pregnant and lactating rats have demonstrated major effects on short and long term functional outcomes while pup weight at birth was not always reduced (Armitage et al. 2004; Zambrano et al. 2005a,b). Thus our findings further sustain the view that weight, either of the whole body or individual organs, is an inadequate measure of compromised fetal development and more refined measures of body composition are needed to assess consequences of maternal nutrient reduction on fetal and neonatal phenotype.
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