Although cobalamin (vitamin B12) was isolated almost 60 years ago, its biochemical,
physiologic and neurologic effects remain incompletely defined. New observations suggest …

The final unique stage in the metabolism of L-isoleucine involves the cleavage of 2-
methylacetoacetyl-CoA to acetyl-CoA and propionyl-CoA (Section 10.4). The propionyl-CoA …

The following review indicates that the impact of cobalamin on neurologic disease extends
far beyond the traditional myelopathy of classical pernicious anemia. The delineation of a …

Background/Aims: Elevated concentration of plasma homocysteine (tHcy) is common in
renal patients, however, the reason behind the resistance to vitamin B 12 and folate therapy …

In humans, poor nutrition, malabsorption and variation in cobalamin (vitamin B12) metabolic
genes are associated with hematological, neurological and developmental pathologies …

Background: Thyroid follicular cells have physiologically high levels of reactive oxygen
species because oxidation of iodide is essential for the iodination of thyroglobulin (Tg) …

The conversion of cyanocobalamin to adenosyl-and methylcobalamin is impaired in
cobalamin-deficient cultured human glial cells. In contrast cultured human skin fibroblasts …

Abstract Hydroxocobalamin (OH-Cbl), when used to treat vitamin B12 deficiency, is better
retained by the body than is cyanocobalamin (CN-Cbl), but the availability to cells has not …

Abstract Cobalamin (Cbl, vitamin B 12) bound to transcobalamin II (TCII) enters cultured
fibroblasts by receptormediated endocytosis. Following degradation of the TCII, Cbl is …

Abstract Transcobalamin II (TC II) deficiency is a rare autosomal recessive disease leading
to cobalamin (Cbl; Vitamin B12) deficiency characterized by failure to thrive, megaloblastic …