Abstract :
[en] Improving sow reproductive performance is an important goal for pig production, especially in China, where reproductive efficiency still lags behind that of some developed countries. In pigs, litter size is not determined only by ovulation rate, but is largely limited by embryonic and fetal survival during gestation. Because a large proportion of embryonic loss occurs during early gestation, especially around the peri-implantation period, this stage is considered an important window for nutritional regulation. Protein and amino acids are essential substrates for maternal tissue recovery, embryo development, placental growth, and fetal development. Therefore, increasing dietary protein supply during early gestation may be a potential strategy to improve reproductive performance in modern highly prolific sows. However, whether dietary protein levels within the commercial range can improve litter performance in multiparous sows, and how maternal dietary protein nutrition affects maternal metabolism, placental function, and fetal development, remain unclear.
Firstly, to evaluate whether dietary protein levels within the commercial range during early gestation could improve reproductive performance in multiparous sows, sows were fed diets containing 12%, 13.5%, or 15% crude protein (CP) from gestational day 0 (GD 0) to GD 30. Reproductive performance and body condition-related indicators were recorded, maternal blood samples were collected at GD 28, and placental samples were collected at farrowing. Serum hormones, serum biochemical indices, oxidative stress markers, inflammatory cytokines, and serum amino acid profiles were measured at GD 28. Placental oxidative stress markers, ATP content, and the expression of genes related to antioxidant defense, mitochondrial function, and nutrient transport were examined at farrowing. The results showed that increasing dietary protein levels from 12% to 15% during early gestation did not significantly improve litter size, live-born rate, or placental functional indicators at farrowing. However, the high protein (HP) diet altered maternal serum amino acid profiles and induced changes in serum alanine aminotransferase (ALT) activity and redox-related indicators at GD 28. These findings suggest that, in multiparous sows, moderate changes in dietary protein within the commercial range may not further improve litter performance when basal protein and amino acid requirements are already met, whereas maternal metabolic status is more sensitive to changes in protein supply.
Based on the observation that dietary protein variation in sows mainly affected maternal metabolic responses rather than litter performance, a mouse model was further used to explore the effects of stronger protein imbalance on early implantation-related regulation, fetal development, placental function, and maternal-fetal nutrient distribution. At GD 6.5, implantation number was not significantly affected by maternal dietary protein level. However, protein imbalance altered maternal serum hormones and lipid-related indicators, ovarian steroidogenesis-related genes, and hormone receptor expression at implantation sites, suggesting that early endocrine and local implantation-related responses were more sensitive than implantation number itself. At GD 18.5, fetal number was not significantly changed, but the HP treatment reduced fetal weight and placental efficiency. These changes were accompanied by altered maternal serum amino acid profiles, non-synchronous changes in amino acid profiles among maternal serum, amniotic fluid, and fetal serum, increased blood urea nitrogen (BUN) in maternal serum, amniotic fluid, and fetal serum, reduced fetal serum glucose, placental oxidative stress, altered mitochondrial function, changes in nutrient transport-related genes, and altered fetal hepatic expression of genes related to glucose and amino acid metabolism. These results indicate that implantation number and fetal number may be relatively robust to maternal dietary protein variation, whereas fetal growth, maternal metabolic homeostasis, and placental function are more sensitive to stronger high-protein/low-carbohydrate nutritional imbalance.
Because the protein studies indicated that maternal metabolic status and placental functional adaptation were more sensitive to nutritional changes than litter size itself, Chenodeoxycholic acid (CDCA) was further used as a metabolism-targeted nutritional intervention during early gestation. This experiment aimed to evaluate whether improving maternal metabolic status during early gestation could exert sustained effects on maternal health and reproductive performance in late gestation. Sows were supplemented with CDCA during early gestation. At GD 110, maternal serum inflammatory cytokines, oxidative stress indicators, antioxidant capacity, glucose- and insulin-related metabolic indicators, serum metabolomic profiles, and fecal microbial composition were evaluated. Reproductive performance was recorded at farrowing. The results showed that early-gestation CDCA supplementation reduced maternal inflammatory responses and oxidative stress, enhanced antioxidant capacity, and improved insulin-related metabolic status at GD 110. Serum metabolomic analysis showed that CDCA affected metabolites related to lipid metabolism, amino acid metabolism, antioxidant responses, and inflammatory regulation. Fecal microbiota analysis showed that CDCA altered gut microbial composition, and correlation analyses suggested associations among specific microbial taxa, serum metabolites, inflammatory markers, oxidative stress indicators, insulin sensitivity, and reproductive performance. Importantly, CDCA supplementation increased total born and live-born piglets without reducing individual live-born piglet weight. These results suggest that early-gestation CDCA supplementation may improve late-gestation maternal physiological homeostasis and reproductive performance, possibly through the regulation of gut microbiota-host metabolic interactions, redox balance, inflammatory status, and insulin-related metabolism.
Overall, this thesis supports the view that maternal metabolic homeostasis is an important regulatory axis linking early-gestation nutritional input, placental functional adaptation, fetal development, and pregnancy outcomes. The sow protein trial showed that increasing dietary protein within a commercial range during early gestation did not necessarily improve litter performance in multiparous sows, but induced maternal metabolic responses. The mouse model further demonstrated that stronger and sustained high-protein/low-carbohydrate nutritional imbalance may exceed placental adaptive capacity, disturb placental redox homeostasis, mitochondrial function, and nutrient transport, and impair fetal growth. The CDCA trial suggested that targeting maternal metabolic homeostasis during early gestation may improve maternal health and reproductive performance later in pregnancy. These findings indicate that future gestational nutrition strategies for sows should move beyond simply increasing CP supply and should instead focus on appropriate protein and amino acid balance, maintenance of maternal metabolic homeostasis, placental functional adaptation, and metabolism-targeted interventions. Such strategies may contribute to improving sow reproductive efficiency, maternal-fetal health, and sustainable pig production.
