The Effects of Iron Deficiency on Blood to Brain Transport in Developing Rats

Abstract

Iron deficiency is the most prevalent micronutrient deficiency in the world and is the major cause of iron deficiency anemia (IDA). IDA may cause motor, cognitive, and psychological dysfunction in infants and pre-school children. The impact of gestational and neonatal iron deficiency-induced angiogenesis/vasculogenesis on the neurovascular unit (NVU) integrity and functionality is still unknown. My central hypothesis is that developmental IDA leads to brain hypoxia and resultant impacts on the NVU including altered vascular permeability and blood-to-brain transport rates of nutrients, metabolites, and hormones. The results presented here tested this hypothesis and I found that iron deficiency increases glucose, lactate, and thyroxine blood-to-brain transport rates in neonatal rats. The NVU is not disrupted in iron-deficient neonatal rats. These findings provide insight into the pathophysiology of brain disorders related to iron deficiency and chronic hypoxia and contribute to our understanding of blood-to-brain transport in the chronic hypoxic and IDA developing brain.