Methyl-Donor Micronutrient for Gestating Sows: Effects on Gut Microbiota and Metabolome in Offspring Piglets

Abstract

This study aimed to investigate the effects of maternal methyl-donor micronutrient supplementation during gestation on gut microbiota and the fecal metabolic profile in offspring piglets. Forty-three Duroc × Erhualian gilts were assigned to two dietary groups during gestation: control diet (CON) and CON diet supplemented with MET (folic acid, methionine, choline, vitamin B6, and vitamin B12). The body weights of offspring piglets were recorded at birth and weaning. Besides this, fresh fecal samples of offspring piglets were collected at 7, 14, and 21 days. The gut microbiota composition, metabolic profile, and short-chain fatty acid (SCFA) profiles in the fecal samples were determined using 16S rDNA sequencing, liquid chromatography-mass spectrometry metabolomics, and gas chromatography methods, respectively. The results showed that maternal methyl-donor micronutrient supplementation increased the microbiota diversity and uniformity in feces of offspring piglets as indicated by increased Shannon and Simpson indices at 7 days, and greater Simpson, ACE, Chao1 and observed species indices at 21 days. Specifically, at the phylum level, the relative abundance of Firmicutes and the Firmicutes to Bacteroidetes ratio were elevated by maternal treatment. At the genus level, the relative abundance of SCFA-producing Dialister, Megasphaera, and Turicibacter, and lactate-producing Sharpea as well as Akkermansia, Weissella, and Pediococcus were increased in the MET group. The metabolic analyses show that maternal methyl-donor micronutrient addition increased the concentrations of individual and total SCFAs of 21-day piglets and increased metabolism mainly involving amino acids, pyrimidine, and purine biosynthesis. Collectively, maternal methyl-donor micronutrient addition altered gut microbiota and the fecal metabolic profile, resulting in an improved weaning weight of offspring piglets.

Non-12α-Hydroxylated Bile Acids Improve Piglet Growth Performance by Improving Intestinal Flora, Promoting Intestinal Development and Bile Acid Synthesis

“…SCFAs are essential metabolites produced by intestinal microbiota, among which acetic acid, propionic acid and butyric acid account for 90% of SCFAs produced by intestinal microbiota [44]. In the detection of intestinal flora, we found that adding NBAs increased the relative abundance of Lactobacillus and Dialister, and both Lactobacillus and Dialister could increase the content of SCFAs [45,46]. Lactobacillus can use carbohydrates in the gut to produce lactic acid.…”

Maternal folic acid and vitaminB12supplementation during medium to late gestation promotes fetal development via improving placental antioxidant capacity, angiogenesis and amino acid transport

“…12 Accumulating evidence also suggests that maternal FV consumption increases SAM levels in both mothers and offspring. 15,39 SAM, a metabolite of Met, disrupts the SAMTOR-GATOR1 complex, thereby activating mTORC1 signaling. 40 Therefore, we speculate that FV supplementation may promote SAM production through remethylation pathways, consequently activating the mTORC1 signaling pathway.…”

“…Our previous research has demonstrated that Met protects cells and supports organ development in combating oxidative stress by elevating SAM levels 12 . Accumulating evidence also suggests that maternal FV consumption increases SAM levels in both mothers and offspring 15,39 . SAM, a metabolite of Met, disrupts the SAMTOR‐GATOR1 complex, thereby activating mTORC1 signaling 40 .…”

“…14 Some studies have exclusively focused on investigating the impact of maternal supplementation with FA and other methyl donors on offspring development and health. 15,16 Little is known about the mechanisms underlying the influence of maternal FV status on placental antioxidant capacity. While FV supplementation may represent an intriguing avenue to directly regulate physiological processes, such as embryonic development during pregnancy, 17,18 its underlying molecular mechanisms in fetal growth and placental function have received limited attention.…”

“…Furthermore, preliminary research has indicated that FV supplementation enhanced embryonic development by reducing the incidence of early pregnancy loss, 13 demonstrating that the reproductive capacity of early parity sows was constrained by insufficient FV levels 14 . Some studies have exclusively focused on investigating the impact of maternal supplementation with FA and other methyl donors on offspring development and health 15,16 . Little is known about the mechanisms underlying the influence of maternal FV status on placental antioxidant capacity.…”