QUICK RECOVERY OF MOUSE PUPS FROM ANEMIA AFTER MATERNAL IRON DEFCIENCY DURING PREGNANCY

Pregnancy is a physiological condition frequently associated with iron deficiency (ID). The causes of ID are high iron demand and its insufficient supply due to low preconception maternal iron reserves and inadequate dietary intake. Here, using a mouse model of ID in pregnancy, we attempted to determine in a time-course study (11 postnatal days), molecular mechanisms of postnatal recovery of mouse pups after gestational ID. Females fed low iron diet 2 weeks prior to mating, and throughout pregnancy, and their progeny showed clear symptoms of ID anemia. Switching anemic mothers to an iron-replete diet just after delivery resulted in a progressive recovery of their progeny from IDA. On postnatal day 11, RBC indices and iron plasma parameters of pups born to anemic mothers were close to those of pups born to iron-replete females. Higher hepatic ferroportin (Fpn) level in the offspring of anemic mothers strongly suggests that the liver despite decreased iron content still remains a source of iron to meet erythropoietic demand. To check the role of duodenal Fpn in iron delivery to the circulation in iron-deficient pups, we assessed its localization and expression in the duodenum. Fpn was located along the basolateral membranes of absorptive enterocytes in 3-day-old anemic pups and its expression was strongly up-regulated compared to age-mate iron-replete pups showing virtually no Fpn staining. We propose that relatively quick normalization of RBC status in pups born to anemic mothers is due to the efficient mobilization of iron from both exogenous and endogenous sources. Supported by NCN/2020/39/B/NZ5/02469.