Maternal iron deficiency alters the expression of glucose transporters in offspring.

Iron deficiency anemia is a major health problem worldwide. Iron is an essential micronutrient in the human body; its demand increases with fetal growth and gestation. Although it has been reported that glucose metabolism is also affected by iron deficiency, only few studies have investigated the influence of iron deficiency during gestation and in offspring. In this study, glucose metabolism in newborns was investigated in terms of maternal iron deficiency prior to pregnancy in a rat model. Briefly, rats were divided into control (CL) and iron deficiency (ID) groups. The levels of serum glucose and insulin and the protein expression of liver GLUT2 in neonates born to dams in the ID group increased. In contrast, the mRNA and protein expression levels of GLUT2 and GLUT4 in the skeletal muscle tended to decrease. In addition, the expression of p-Akt (Thr308), which is involved in GLUT4 membrane translocation, decreased, suggesting that GLUT4 translocation to the plasma membrane may not have been sufficiently promoted. These results suggest that maternal iron deficiency may influence glucose metabolism in neonates and potentially increase the risk of developing metabolic abnormalities and lifestyle-related diseases later in life.