PSXIV-22 Impact of Maternal Plane of Nutrition in Combination with Strategic One-Carbon Metabolites Supplementation During Early Pregnancy on Vascularity and Cell Proliferation in the Fetal Small Intestine

Abstract

Abstract Objective of our study were to investigate the impact of maternal nutrition during early pregnancy on the vascularity and proliferation of fetal intestine and whether supplementing one-carbon metabolites (OCM) could mitigate any changes arising from altered maternal nutrition. We used a 2 x 2 factorial arrangement of treatments with two levels of heifer gain: control (CON; 0.45 kg/d) and restricted (RES; -0.23 kg/d), with and without (+/- OCM) supplementation. Crossbred Angus beef heifers were estrous synchronized and bred via artificial insemination with single-sire female-sexed semen. Heifers were divided into four nutritional treatments (n = 8 ± 1 per treatment) at breeding. Targeted heifer gain (achieved by changing in intake of a common diet) and OCM treatments were administered from d 0 to 63 of gestation and then all heifers were fed a common diet targeting 0.45 kg/d gain. Treatments containing OCM were given rumen-protected methionine (10 g/d) and choline (60 g/d) in a fine-ground corn carrier administered daily, with weekly injections of folate (320 mg) and vitamin B12 (20 mg). The non-supplemented treatment (-OCM) received the corn carrier and saline injections. On day 161 of gestation heifers were harvested and samples were collected from fetal jejunum for analysis. Vascularity was assessed via measurement of capillary density using anti-CD31 and anti-CD34 fluorescent staining. Cell proliferation within intestinal tissues was assessed by KI-67 fluorescent staining. Images were analyzed using ImagePro-Premiere software. Maternal gain × OCM interactions were not present (P > 0.11). Fetuses from restricted dams had greater (P = 0.05) capillary area density in the villi compared with CON (5.48 vs. 4.72 ± 0.38%), while OCM had no effect. Crypt and total cell proliferation were greater (P < 0.05) in CON. Providing OCM reduced (P = 0.01) total intestinal cell proliferation. The observed increase in capillary density in the villi of fetuses from restricted dams may be a compensatory response to reduced maternal nutrient availability, aimed at preparing the offspring for increasing post-natal nutrient delivery. Conversely, the decreased proliferation in crypt cells appears to be a logical response to restricted nutrition and may indicate a slowing of the rate of cell division, which could have long-term consequences for intestinal development. Our results also demonstrate that maternal OCM can reduce total intestinal cell proliferation in the fetal intestine, regardless of maternal nutrition. One-carbon metabolites have crucial roles in DNA methylation and other cellular processes for proper cellular function and development. Observed decreases resulting from the provision of OCM may indicate enhanced energetic efficiency, reduced epithelial cell turnover, and/or reduce apoptotic events in the villa. Further studies are needed to determine the long-term effects of maternal OCM on fetal intestinal development and function. USDA is an equal opportunity provider and employer.