title: Advanced glycation end products overload might explain intracellular cobalamin deficiency in renal dysfunction, diabetes and aging.
abstract: Advanced glycation end products (AGEs) contribute to aging. Cobalamin (Cbl) is required for cell growth and functions, and its deficiency causes serious complications. Diabetics and renal patients show high concentrations of Cbl, but metabolic evidence of Cbl deficiency that is reversible after Cbl treatment. Cbl might be sequestered in blood and cannot be delivered to the cell. Megalin mediates the uptake of transcobalamin-Cbl complex into the proximal tubule cells. Megalin is involved in the uptake and degradation of AGEs. In aging, diabetes or renal dysfunction, AGEs might overload megalin thus lowering Cbl uptake. Transcobalamin-Cbl might retain in blood. Shedding of megalin and transcobalamin receptor under glycation conditions is also a possible mechanism of this phenomenon.
authors: Department of Clinical Chemistry and Laboratory Medicine, University Hospital of Saarland, 66421 Homburg, Germany. rima.obeid@uniklinikum-saarland.de
authors: Rima
authors: R
authors: Obeid
authors: Batool
authors: B
authors: Shannan
authors: Wolfgang
authors: W
authors: Herrmann
mesh_terms: D000368:Aged; D000375:Aging / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000378:metabolism*; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D007687:Kidney Tubules, Proximal / Q000503:physiopathology*; D015416:Maillard Reaction; D014805:Vitamin B 12 / Q000378:metabolism*; D014806:Vitamin B 12 Deficiency / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D017127:Glycation End Products, Advanced; D014805:Vitamin B 12