Effects of dietary supplementation of gestating sows with adenosine 5'-monophosphate or adenosine on placental angiogenesis and vitality of their offspring

Abstract

Our previous study found that dietary nucleotide supplementation, including adenosine 5'-monophosphate (AMP), could increase AMP content in sow milk and promote piglet growth, but its effects on placental efficiency and piglet vitality remain unknown. This experiment aimed to investigate the effects of dietary AMP or its metabolite adenosine (ADO) supplementation on sow reproductive performance and placental angiogenesis. A total of 135 sows with a similar farrowing time were blocked by backfat and body weight (BW) at day 65 of gestation and assigned to one of three dietary treatment groups (n = 45 per treatment): basal diet, basal diet supplemented with 0.1% AMP or 0.1% ADO, respectively. Placental analysis and the characteristics of sows and piglets unveiled that compared with control (CON) group, AMP or ADO supplementation could improve sow placental efficiency (P < 0.05) and newborn piglet vitality (P < 0.05), increase piglet birth weight (P < 0.05), and reduce stillbirth rate (P < 0.05). More importantly, AMP or ADO supplementation could increase the contents of AMP, ADO, and their metabolites in placentae (P < 0.05). Meanwhile, AMP or ADO supplementation could also increase placental vascular density (P < 0.05) and the expression of vascular endothelial growth factor A (P < 0.05), as well as promote the migration and tube formation of porcine iliac artery endothelial cells (P < 0.05). Overall, maternal dietary AMP or ADO supplementation could increase their contents in the placenta, thereby improving placental angiogenesis and neonatal piglet vitality.

Keywords: adenosine; adenosine 5ʹ-monophosphate; angiogenesis; piglet vitality; placenta.

Figure 1.

Effects of AMP and ADO supplementation on reproductive performance of sows. (A) Placental efficiency. (B) Piglet vitality. (C) Coefficient of variation between litters. (D) Stillbirth rate. All data are presented as the mean ± SEM. Each sow or litter was regarded as an experimental unit (n = 44, 45, 43). A–B, columns with different large letters mean significant differences at P < 0.05.

Figure 2.

Effects of AMP and ADO supplementation on concentrations of AMP, ADO, and their downstream metabolites in placental tissue (A–H): ADO (A), Adenine (B), AMP (C), SAH (D), Xanthine (E), Hypoxanthine (F), Inosine (G), and Uric Acid (H). All data are presented the mean ± SEM. Each placenta tissue was regarded as an experimental unit (n = 6 per group) A–B, columns with different large letters mean significant differences at P < 0.05.

Figure 3.

Effects of AMP and ADO supplementation on placental angiogenesis. Each placenta tissue was regarded as an experimental unit (n = 6 per group). (A and B) Hematoxylin and eosin staining analysis of blood vessel density in CON, ADO, and AMP placental tissues, with black arrows indicating placental blood vessels. (C–E) Real-time PCR and Western blot analysis of mRNA and protein expression of angiogenesis-related factors in placentae. All data are presented as mean ± SEM. A–B, columns with different large letters mean significant differences at P < 0.05.

Figure 4.

Effects of AMP and ADO supplementation on PIECs tube formation and migration. (A and B) Representative images of tube formation by PIECs. (C and D) Wound healing assay in each group. (E–G) Western blot analysis of VEGF-A protein expression in PIECs. All data are presented as mean ± SEM. Each Petri dish with cells is considered as one experimental unit (n = 4 per group). A–B, columns with different large letters mean significant differences at P < 0.05.