Two experiments evaluated the ability of maternal fatty acid supplementation to alter conceptus and endometrial fatty acid composition. In Exp. 1, treatments were 1) the control, a corn-soybean meal diet; 2) flax, the control diet plus ground flax (3.75% of diet); and 3) protected fatty acids (PFA), the control plus a protected fish oil source rich in n-3 PUFA (Gromega, JBS United Inc., Sheridan, IN; 1.5% of diet). Supplements replaced equal parts of corn and soybean meal. When gilts reached 170 d of age, PG600 (PMSG and hCG, Intervet USA, Millsboro, DE) was injected to induce puberty, and dietary treatments (n = 8/treatment) were initiated. When detected in estrus, gilts were artificially inseminated. On d 40 to 43 of gestation, 7 gilts in the control treatment, 8 gilts in the PFA treatment, and 5 gilts in the flax treatment were pregnant and were slaughtered. Compared with the control treatment, the flax treatment tended to increase eicosapentaenoic acid (EPA: C20:5n-3) in fetuses (0.14 vs. 0.25 +/- 0.03 mg/g of dry tissue; P = 0.055), whereas gilts receiving PFA had more (P < 0.05) docosahexaenoic acid (DHA: C22:6n-3) in their fetuses (5.23 vs. 4.04 +/- 0.078 mg/g) compared with gilts fed the control diet. Both the flax and PFA diets increased (P < 0.05) DHA (0.60, 0.82, and 0.85 +/- 0.078 mg/g for the control, flax, and PFA diet, respectively) in the chorioallantois. In the endometrium, EPA and docosapentaenoic acid (C22:5n-3) were increased by the flax diet (P < 0.001; P < 0.05), whereas gilts receiving PFA had increased DHA (P < 0.001). The flax diet selectively increased EPA, and the PFA diet selectively increased DHA in the fetus and endometrium. In Exp. 2, gilts were fed diets containing PFA (1.5%) or a control diet beginning at approximately 170 of age (n = 13/treatment). A blood sample was collected after 30 d of treatment, and gilts were artificially inseminated when they were approximately 205 d old. Conceptus and endometrial samples were collected on d 11 to 19 of pregnancy. Plasma samples indicated that PFA increased (P < 0.005) circulating concentrations of EPA and DHA. Endometrial EPA was increased (P < 0.001) for gilts fed the PFA diet. In extraembryonic tissues, PFA more than doubled (P < 0.001) the EPA (0.13 vs. 0.32 +/- 0.013 mg/g) and DHA (0.39 vs. 0.85 +/- 0.05 mg/g). In embryonic tissue on d 19, DHA was increased (P < 0.05) by PFA (0.20 vs. 0.30 +/- 0.023 mg/g). Supplementing n-3 PUFA, beginning 30 d before breeding, affected endometrial, conceptus, and fetal fatty acid composition in early pregnancy. Dynamic day effects in fatty acid composition indicate this may be a critical period for maternal fatty acid resources to affect conceptus development and survival.

A total of 59 gilts were used to determine the effects of supplemental L-carnitine on reproductive performance. Experimental treatments were arranged in a 2 Ã-3 factorial with main effects of L-carnitine (0 or 50 ppm) and day of gestation (40, 55, or 70). All gilts received a constant feed allowance of 3.86 lb/day and a top-dress containing either 0 or 88 mg of L-carnitine, starting on the first day of breeding and continuing until the day of harvest. Total litter size, total litter weight, and crown-to-rump length of fetuses were not different (P>0.10) between treatments at any gestation length. By d 70 of gestation, average fetus weight was heavier (P = 0.06) for fetuses from gilts fed L-carnitine, compared with fetuses from gilts fed the control diet. In addition, at d 70, fetal insulin-like growth factor-II (IGF-II) concentrations were lower (P = 0.09) for fetuses from gilts fed L-carnitine than for fetuses from gilts fed the control diet. Feeding L-carnitine may have decreased fetal IGF-II, therefore increasing cell proliferation and delaying cell differentiation. These results show that providing supplemental Lcarnitine to gestating gilts has beneficial effects on average fetal weight, possibly observed because of its ability to reduce fetal IGF-II concentrations. SummaryA total of 59 gilts were used to determine the effects of supplemental L-carnitine on reproductive performance. Experimental treatments were arranged in a 2 × 3 factorial with main effects of L-carnitine (0 or 50 ppm) and day of gestation (40, 55, or 70). All gilts received a constant feed allowance of 3.86 lb/day and a top-dress containing either 0 or 88 mg of L-carnitine, starting on the first day of breeding and continuing until the day of harvest. Total litter size, total litter weight, and crown-to-rump length of fetuses were not different (P>0.10) between treatments at any gestation length. By d 70 of gestation, average fetus weight was heavier (P = 0.06) for fetuses from gilts fed L-carnitine, compared with fetuses from gilts fed the control diet. In addition, at d 70, fetal insulin-like growth factor-II (IGF-II) concentrations were lower (P = 0.09) for fetuses from gilts fed L-carnitine than for fetuses from gilts fed the control diet. Feeding L-carnitine may have decreased fetal IGF-II, therefore increasing cell proliferation and delaying cell differentiation. These results show that providing supplemental Lcarnitine to gestating gilts has beneficial effects on average fetal weight, possibly observed because of its ability to reduce fetal IGF-II concentrations.