The placenta and fetal intestines are two key nutrient transport organs that sustain and nurture growing fetus. Insufficient placental development and consequently inadequate fetal nutrient supply can lead to IUGR resulting in low birth weight offspring. Our experimental objectives were to investigate the effects of elevated maternal nutrition, IUGR, and E2 supplementation during mid-gestation (in an attempt to rescue IUGR offspring) on placental and fetal intestinal cell proliferation, angiogenic gene expression, and vascularity. Limited responsiveness in placental development and vascularization to E2 supplementation was observed, likely due to inappropriate timing or dose of E2. However, maternal E2 supplementation increased fetal small intestinal length and GUCY1b3 mRNA expression, suggesting that E2 supplementation has positive effects on IUGR fetal intestinal growth. In conclusion, understanding molecular mechanisms associated with IUGR and possible effects of E2 supplementation in rescuing IUGR may lead to enhanced human health and livestock production efficiency.

published_or_final_version / abstract / toc / Physiology / Master / Master of Philosophy

The effects of maternal dietary glucose restriction on reproductive performance were investigated by feeding pregnant rats isocaloric diets containing graded levels of dietary glucose (0, 12, 24 and 60%) during pregnancy and during pregnancy and lactation, and by measuring the effects of glucose restriction on (1) maternal, fetal and neonatal metabolism, on (2) growth and composition of the mammary glands and placentas, and (3) on milk composition. Carbohydrate restriction induced maternal metabolic adaptations that were proportional to the severity of the glucose restriction. Placental growth and composition as well as mammary gland composition were not affected by dietary glucose restriction, whereas fetal growth and development and milk composition were significantly impaired when glucose was limited in the maternal diet. This suggests that the effects of dietary glucose on the fetus and on milk composition were not mediated by changes in placenta and mammary gland DNA, protein or glycogen concentrations. Complete dietary glucose restriction significantly depressed fetal liver, lung and heart glycogen concentrations; repletion of the maternal diets with 12 and 24% glucose restored cardiac glycogen to normal but not fetal lung glycogen and liver glycogen. Pups born to dams fed a glucose-free diet failed to survive longer than 24 h postpartum and that was associated with the low levels of tissue glycogen at birth in these pups. At birth, lung and liver glycogen concentration of pups of the 12 and 24% glucose diets was similar to pups of the control diet despite the fact that these reserves were depressed in utero; and these pups efficiently corrected the transient hypoglycemia observed following parturition. The effects of glucose restriction on fetal liver glycogen were not reflected by similar changes in fetal plasma insulin, glucagon and glucose levels or in glycogen synthase and phosphorylase activities. Maternal dietary glucose was an important determinant

No description available.

The effect of maternal dietary glucose on perinatal phosphoenolpyruvate carboxykinase (PEPCK) gene expression was investigated in this study. Pregnant rats were fed isoclaoric diets containing graded levels of glucose (0%, 12%, 24% and 60%) from gestation day 2 to lactation day 15. The developmental profiles of PEPCK gene expression in fetal and neonatal liver and kidney were analyzed by northern blot. In the liver, feeding glucose free and glucose restriction (12% and 24%) diets precociously induced PEPCK gene expression at day 21 of gestation. In the kidney, PEPCK mRNA (2.8 kb) was detected at birth in the glucose free group, 12-16 hours postnatally in control group; it was not visualized until day 3 in the 12% and 24% glucose restriction groups. In our study, two species of RNA (1.8 kb and 2.8 kb) were hybridized with PEPCK cDNA probes, and there was a relationship between maternal dietary glucose levels and the 1.8 kb RNA fragment in the kidney.

No description available.

Obese, female Spraque-Dawley rats were assigned, on a weight basis, to one of three dietary treatments: ad lib, 15% caloric restriction, and 30% caloric restriction. All other nutrients were fed at levels to meet dietary requirements. Each treatment groups was further sub-divided into pregnant and non-pregnant animals. Rats were sacrificed on Day 20 of gestation and fetuses were taken by Caesearean section. Maternal and fetal body composition, maternal serum protein concentrations were examined. Weight change for pregnant rats was +85 gms in the ad lib-fed group, +82 gms in the 15% calorie restricted group, and +56 gms in the 30% calorie restricted group. Weight changes for the non-pregnant rats for 20 days of dietary treatment were +53 gms, +18 gms, and -7 gms respectively. Fetal body nitrogen and average pup weight did not differ between treatment groups. Total maternal body nitrogen was not decreased during pregnancy in ad lib-fed and 15% calorically restricted animals. It did decrease in 30% calorically restricted animals. Ad lib-fed animals showed no changes in total body fat. Animals on the 15% calorie restriction diet showed no change in total body fat percentages. Animals on the 30% calorie restriction showed a 10% decrease in total body fat content as compared to the ad lib and 15% restricted pregnant group. Serum protein levels decreased in pregnant animals as caloric restriction increased. Serum protein levels in nonpregnant animals increased as dietary restriction increased. The fetal compartment was not affected by maternal caloric restriction up to 30% provided that all other nutrients were adequate. Maternal stores were affected at a level of 30% caloric restriction. / Master of Science