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Miyako Furuta, Toshiya Funabashi, Tatsuo Akema, Maternal Iron Deficiency Heightens Fetal Susceptibility to Metabolic Syndrome in Adulthood, Endocrinology, Volume 153, Issue 3, 1 March 2012, Pages 1003–1004, https://doi.org/10.1210/en.2011-2116
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Iron is involved in the functional conformation of hemoglobin; it facilitates hemoglobin binding to oxygen. Iron also has a critical role in erythropoiesis. When erythroblasts proliferate and differentiate, they require large amounts of iron for hemoglobin synthesis. The heme moiety of erythroblasts requires iron for synthesis, and it regulates globin production. Thus, iron deficiency (ID) causes anemia, which is associated with many diseases. Because ID in the adult has a detrimental influence on erythrocyte function, maternal ID affects fetal development; thereafter, many physiological functions may be altered in the offspring.
In rats fed a low-iron diet, although maternal ID did not cause severe anemia in the dam, brain development in the offspring was profoundly impaired; their offspring showed an increased auditory brainstem response time later in life, which suggested an impairment in brain development (1). Thus, subclinical anemia in the mother during early pregnancy may be a risk factor for abnormal central nervous system development in the fetus. The authors also showed that there was a time window for the susceptibility of brain development to ID (1). The fetal stage was thought to be the most vulnerable stage during development (2). The bottom line was that, when a fetus had experienced maternal ID, health problems become manifest in adulthood, despite adequate adult nutrition.
