PSIV-B-26 Late-Breaking: Polyunsaturated fatty acids and methionine supplementation during late gestation alters fetal liver development in sheep

Abstract

Abstract Supplementation with polyunsaturated fatty acids or methionine have a fetal programming effect in mammals. However, the effect of both nutrients on fetal development and DNA methylation have not been explored. The objective of this study was to evaluate the effects of supplementing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), methionine, or both to ewes during late gestation on fetus development and liver global DNA methylation. Twenty ewes (n = 5) were supplemented from day 100 to 145 of gestation. The treatments were: 1) control diet (CONT) without EPA and DHA supplementation (PUFA) or methionine supplementation (MET); 2) control plus PUFA (1 % Ca salts of fatty acids intake, Strata G113®); 3) control plus MET (0.1 % rumen protected methionine intake, Smartamine®); and 4) control plus PUFA and MET (PUFA+MET). On day 145, ewes were euthanized and fetuses were removed. Ewe, fetus, placenta, and fetal liver were weighed. Plasma samples were collected from ewes and fetuses to measure concentration of glucose and NEFA. Liver global DNA methylation was analyzed. Data was analyzed as a complete randomized experiment with a 2x2 factorial arrangement of treatments. Ewe supplementation did not affect (P > 0.1) fetus and placental weight. There was an interaction of treatment effect (P = 0.02) on fetal liver weight and ewe BW; CONT and PUFA+MET were grater that PUFA and MET. There were no differences (P > 0.10) on ewe and fetus NEFA as well as fetus glucose, but MET increased (P = 0.03) ewe plasma glucose concentration. Both treatments affected liver global DNA methylation of fetus (main effects P < 0.01; interaction P = 0.32); all the treatments increased global DNA methylation compared, with CONT, and PUFA+MET has greater than PUFA and MET. In conclusion PUFA and methionine supplementation in late gestation modified fetus liver development and DNA methylation.