Placental adaptations in response to protein restricted diet.

GASPEROWICZ M.; GONZALEZ P.; HALLGRIMSSON B; CROSS J

Congreso; Latin American Association for Maternal-Fetal Interaction and Placenta-SLIMP; 2013

Embryonic growth in mammals is dependent on maternal supply of nutrients mediated by the placenta. When the availability of nutrients is limited, the mechanisms that regulate resource allocation constitute key determinants of maternal and fetal survival. Adaptive responses in placental phenotype are expected to enhance the robustness of fetal development and increase the chances of maternal survival. This study investigated the responses of feto-placental development to maternal malnutrition. C57BL/6J female mice (n=60) were fed either a low-protein (LP) diet (6% protein) or a control isocaloric diet (20% protein) starting two weeks before mating and continuing throughout gestation. On embryonic days (E) 10.5, 17.5 and 18.5 conceptuses were dissected and tissue samples prepared for morphometric, stereological and quantitative RT-PCR (qRT-PCR) analyses, which included an array of growth factor genes, amino acid transporters genes, common markers of trophoblast cell subtypes, as well as 8 genes from placenta specific proliferin-related protein family. Our results showed that in LP group, placenta weight was significantly lower already at E10.5, followed by reduction of maternal weight at E17.5, while the fetuses became significantly smaller no earlier than at E18.5, which is usually the very last day of pregnancy. Interestingly at E17.5 the volume of the labyrinth, the placenta layer responsible for feto-maternal exchange, was not changed between LP and control placentas. As well the level of expression of amino acid transporters genes Slc38a4 and Slc38a2 was not significantly different between both groups. However, the junctional zone, a layer rich in energy storing glycogen cells, was significantly smaller in LP placentas. Accordingly qRT-PCR analysis at E10.5 and E17.5 demonstrated a significant reduction in the Pcdh12 gene, a marker of glycogen cells, while there was either an increase or no change at all in the expression levels of markers of the other junctional zone cell subtype – spongiotrophoblast. Therefore we propose that junctional zone of the placenta, and particularly its glycogen cells, might act as an energy buffer between maternal supply and fetal demand, accumulating, in form of glycogen, an excess glucose from maternal blood circulation, and releasing it in the time when embryo needs extensive energy for a rapid growth.