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VITAMIN B-12 (COBALAMIN) IS ESSENTIAL FOR RED BLOOD CELL FORMATION
Moestrup SK (2006). New insights into carrier binding and epithelial uptake of the erythropoietic nutrients
cobalamin and folate. Curr Opin Hematol. 13(3):119-23.
PURPOSE OF REVIEW: In addition to malnutrition several genetic and acquired conditions may
affect the homeostasis of cobalamin (vitamin B12) and folate, leading to megaloblastic anemia and other diseases.
The present review describes new insight into protein handling of cobalamin and folate.
RECENT FINDINGS: The recent solution of the three-dimensional structure of the cobalamin binder
transcobalamin shows two separate domains enclosing the vitamin. This structure apparently also applies for the
other homologous cobalamin binders, intrinsic factor and haptocorrin. Genetic studies of inherited cobalamin
malabsorption and biochemical studies have now revealed that the functional receptor for uptake of intrinsic
factor-vitamin cobalamin complexes also is a complex itself consisting of two different gene products, cubilin and
amnionless. A role in folate uptake of megalin, an endocytic receptor for epithelial uptake of various proteins
including transcobalamin, is now also indicated by the observation that megalin can mediate uptake of soluble
folate receptor.
SUMMARY: New data show the structure of cobalamin carriers and reveal novel proteins involved
in the epithelial uptake of cobalamin and folate. Genetic abnormalities in three different genes encoding proteins
in the epithelial uptake of cobalamin are now known to cause malabsorption of cobalamin and megaloblastic
anemia.
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Koury MJ, Ponka P (2004). New insights into erythropoiesis: the roles of folate, vitamin B12, and
iron. Annu Rev Nutr. 24:105-31.
Erythropoiesis is the process in which new erythrocytes are produced. These new erythrocytes replace the oldest
erythrocytes (normally about one percent) that are phagocytosed and destroyed each day. Folate, vitamin B12, and
iron have crucial roles in erythropoiesis. Erythroblasts require folate and vitamin B12 for proliferation during
their differentiation. Deficiency of folate or vitamin B12 inhibits purine and thymidylate syntheses, impairs DNA
synthesis, and causes erythroblast apoptosis, resulting in anemia from ineffective erythropoiesis. Erythroblasts
require large amounts of iron for hemoglobin synthesis. Large amounts of iron are recycled daily with hemoglobin
breakdown from destroyed old erythrocytes. Many recently identified proteins are involved in absorption, storage,
and cellular export of nonheme iron and in erythroblast uptake and utilization of iron. Erythroblast heme levels
regulate uptake of iron and globin synthesis such that iron deficiency causes anemia by retarded production rates
with smaller, less hemoglobinized erythrocytes.
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