Molecular and Biochemical Basis of Iron Deficiency Anaemia in Neonatal Piglets from Sows with Sub-Optimal Iron Status in Enugu State, South East Nigeria

Iron deficiency anaemia in neonatal piglets is exacerbated in systems where sow iron reserves are suboptimal, yet the molecular and biochemical basis of this maternal-neonatal iron transfer deficiency under Nigerian production conditions has not been systematically investigated. This doctoral study characterised the molecular mechanisms of iron transfer and utilisation deficiency in neonatal piglets from iron-deficient sows at commercial piggeries in Enugu State, South East Nigeria. Forty sows classified as iron-deficient by serum ferritin below 50 ng/mL and forty iron-replete sows were enrolled, with fifty neonatal piglets from each group (two to four piglets per sow) monitored from birth through four weeks. Serum ferritin, iron, transferrin, transferrin saturation, erythropoietin, hepcidin, and divalent metal transporter-1 expression in duodenal biopsy samples from piglets were quantified by immunoassay and real-time PCR. Piglets from iron-deficient sows exhibited significantly lower birth haemoglobin, serum iron, and ferritin, with compensatory upregulation of erythropoietin reaching five times control values by day three. Duodenal divalent metal transporter-1 expression was upregulated fourfold in iron-deficient piglets, confirming an intestinal absorption up-regulation response. Hepcidin was markedly suppressed in iron-deficient piglets, consistent with iron-demand-driven hepcidin downregulation. Mortality was significantly higher in iron-deficient piglet groups through day seven. These original molecular findings provide a comprehensive mechanistic understanding of neonatal iron deficiency in Nigeria and identify hepcidin pathway modulation as a novel therapeutic approach for preventing neonatal piglet anaemia. Keywords: iron deficiency anaemia, piglets, hepcidin, divalent metal transporter, Enugu State.