# Biochemical impact of ALAEm supplementation in late gestation on the reproductive performance of sows

**Authors:** Linlu Zhao, Jin Zhang, Jieyi He, Xingbin Ma, Zhichao Yu, Yanhong Yong, Youquan Li, Xianghong Ju, Xiaoxi Liu

PMC · DOI: 10.3389/fvets.2025.1548263 · Frontiers in Veterinary Science · 2025-04-23

## TL;DR

This study shows that adding a plant extract mix called ALAEm to sows' diets during late pregnancy improves their reproductive performance and placental health.

## Contribution

The study introduces ALAEm as a novel supplement that enhances sow fertility through biochemical and molecular mechanisms in placental tissues.

## Key findings

- ALAEm improved reproductive outcomes like piglet numbers and weaning weights in sows.
- The supplement reduced placental inflammation, oxidation, and apoptosis while promoting growth and nutrient transport.
- ALAEm altered lipid metabolism in placental tissues via alpha-linolenic acid pathways.

## Abstract

Adding plant extracts to diets to enhance sow performance and health is widely regarded as a healthy and sustainable practice. In promoting antibiotic-free farming, plant extracts have emerged as a leading solution for enhancing sow fertility through nutritional strategies. The aim of this study was to investigate the biochemical impacts of supplementation of sows with ALAEm (composed of nine plant extracts) on blood and placental indices of sows in late gestation. The components of ALAEm were determined by UPLC-MS/MS. 196 normal gestation parturient sows were randomly allocated into two groups (n = 98 per group): the control group and the test group fed 20 g/d ALAEm supplementation at 74–114 d of gestation. The study examined the various clinical indexes in the blood, the expression of genes and proteins and metabolomics in the placenta. Dietary ALAEm supplementation improved sow reproductive performance (total number of piglets born alive, number of piglets weaned, wean weight), serum biochemical indices, placental structure and increased gene and protein expression of ZO-1, Claudin-1 and other placental junction-associated factors. ALAEm attenuated placental tissue oxidation, inflammation, and apoptosis, promoted placental growth (EGF and IGF-1) and angiogenesis factors (VEGFA, PIGF and other factors), and increased the nutrient transport in placental (GLUT1 and SNAT2). Dietary ALAEm supplementation decreased the number of metabolites associated with lipid metabolism through alpha-linolenic acid metabolism. Therefore, dietary supplementation of ALAEm in the late gestation may improve fertility by reducing the levels of inflammation, oxidation and apoptosis in placental tissues via the EGFR/VEGFR2-PI3K-AKT1 pathway, promoting placental growth, angiogenesis and nutrient transport, and altering the levels of placental lipid metabolites via α-linolenic acid metabolism.

## Linked entities

- **Genes:** TJP1 (tight junction protein 1) [NCBI Gene 7082], CLDN7 (claudin 7) [NCBI Gene 1366], EGF (epidermal growth factor) [NCBI Gene 1950], IGF1 (insulin like growth factor 1) [NCBI Gene 3479], VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422], PIGF (phosphatidylinositol glycan anchor biosynthesis class F) [NCBI Gene 5281], SLC2A1 (solute carrier family 2 member 1) [NCBI Gene 6513], SLC38A2 (solute carrier family 38 member 2) [NCBI Gene 54407], EGFR (epidermal growth factor receptor) [NCBI Gene 1956], KDR (kinase insert domain receptor) [NCBI Gene 3791], PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) [NCBI Gene 5290], AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207]
- **Proteins:** TJP1 (tight junction protein 1), CLDN7 (claudin 7), EGF (epidermal growth factor), IGF1 (insulin like growth factor 1), VEGFA (vascular endothelial growth factor A), PIGF (phosphatidylinositol glycan anchor biosynthesis class F), SLC2A1 (solute carrier family 2 member 1), SLC38A2 (solute carrier family 38 member 2)
- **Chemicals:** alpha-linolenic acid (PubChem CID 5280934)

## Full-text entities

- **Genes:** EGFR (epidermal growth factor receptor) [NCBI Gene 1956] {aka ERBB, ERBB1, ERRP, HER1, NISBD2, NNCIS}, PIGF (phosphatidylinositol glycan anchor biosynthesis class F) [NCBI Gene 5281] {aka OORS}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, TJP1 (tight junction protein 1) [NCBI Gene 7082] {aka ZO-1}, KDR (kinase insert domain receptor) [NCBI Gene 3791] {aka CD309, FLK1, VEGFR, VEGFR2}, EGF (epidermal growth factor) [NCBI Gene 1950] {aka HOMG4, URG}, SLC38A2 (solute carrier family 38 member 2) [NCBI Gene 54407] {aka ATA2, PRO1068, SAT2, SNAT2}, SLC2A1 (solute carrier family 2 member 1) [NCBI Gene 6513] {aka CSE, DYT17, DYT18, DYT9, EIG12, GLUT}, CLDN1 (claudin 1) [NCBI Gene 9076] {aka CLD1, ILVASC, SEMP1}
- **Diseases:** inflammation (MESH:D007249)

## Full text

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## Figures

10 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12055862/full.md

## References

109 references — full list in the complete paper: https://tomesphere.com/paper/PMC12055862/full.md

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Source: https://tomesphere.com/paper/PMC12055862