Maternal Alkaline-Ionized Mineral Complex Supplementation Regulates Intestinal Epithelial Development and Promotes Glucose and Lipid Metabolism Through the Wnt/Notch Pathway in Piglets.

Breast milk is the sole nutritional source for infants during lactation, but the immaturity of infants' intestinal function elevates the risk of infant malnutrition. As a nutritional additive, maternal Alkaline Ionized Mineral Complex (AIMC) has great application potential in livestock production. This study investigated maternal AIMC supplementation on offspring glucose and lipid absorption using a piglet model. Thirty sows at 107 days of gestation were randomly divided into the Con group (basal diet) or the AIMC group (basal diet + 30 g/head/day AIMC) and fed until piglets were weaned (total 28 days). The results of the study indicated that AIMC increased the sow's milk yield and elevated the contents of lactose and fat in milk. Results from untargeted metabolomics revealed that AIMC regulated the contents of metabolites such as glucose, lactose, 5-Methylcytosine, and thymidine in milk. KEGG analysis found that signaling pathways related to glycolipid metabolism and nucleotide metabolism were enriched. In addition, maternal AIMC supplementation increased the weaning weight of piglets and upregulated the expression of genes related to glucose and lipid metabolism in the jejunum. Mechanistically, maternal AIMC supplementation maintained the proliferation of intestinal epithelial cells (IECs) and promoted the differentiation of intestinal stem cells (ISCs) into absorptive enterocytes by activating the Wnt/Notch signaling pathway. Consequently, maternal AIMC supplementation regulated the proliferation and differentiation of ISCs through the gut-breast axis and the Wnt/Notch signaling pathway, thereby enhancing glucose and lipid metabolism in the intestines of offspring. Our research provides a novel strategy to support intestinal growth and development in neonatal mammals.