Abstract
Either iron excess or iron deficiency may adversely affect growth of pigs. This study assessed the effect of dose of iron supplement on growth and iron metabolism in nursing piglets born small (SGA) or appropriate for gestational age (AGA). Eight SGA piglets (BW=1.18 kg) and 16 AGA piglets (BW=1.73 kg) were enrolled on postnatal day (PD) 1. The SGA piglets orally received high iron supplementation (15 mg/kg·d; SGAH), and AGA piglets orally received either high (15 mg/kg·d; AGAH, n = 6) or low iron supplementation (1 mg/kg·d; AGAL, n = 6) from PD 2 to 21. Body weight was recorded every third day. Blood samples were collected on PD 1, 7, 14, and 21. Liver and duodenal mucosa samples were collected on PD 21 to analyze the mRNA and protein expressions of iron transporters and regulators. All data were analyzed as a randomized complete block design using the PROC MIXED of SAS. The SGA piglets had lower hematocrit and hemoglobin than AGA piglets on PD1 (P < 0.05). The dose of iron supplement did not affect the growth trajectory of nursing piglets. In comparison with AGAL group, high iron increased (P < 0.05) hematocrit, hemoglobin, plasma iron, transferrin saturation, and iron load in duodenal mucosa (DM) and liver on PD 21 regardless of birth BW. High iron reduced the DMT1 and TFRC and increased FTL in DM (P < 0.05). High iron decreased TFRC and increased HAMP in liver (P < 0.05). Hepatic expression of H-ferritin were increased (P < 0.05) by high iron. Despite drastic induction of HAMP in liver, protein expression of ferroportin in DM were unaffected by high iron intake. In conclusion, iron transporters and regulators in liver and gut were coordinately regulated to prevent iron overload, but the hepcidin-ferroportin axis was unresponsive to dietary iron intake.