Department of Clinical Chemistry and Laboratory Medicine, University Hospital of Saarland, 66421 Homburg, Germany.
Med Hypotheses. 2011 Nov;77(5):884-8. doi: 10.1016/j.mehy.2011.08.002. Epub 2011 Aug 30.
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.
晚期糖基化终产物（AGEs）与衰老有关。钴胺素（Cbl）是细胞生长和功能所必需的，其缺乏会导致严重的并发症。糖尿病和肾病患者体内 Cbl 浓度较高，但 Cbl 代谢证据表明，在 Cbl 治疗后可逆转 Cbl 缺乏。Cbl 可能被隔离在血液中，无法输送到细胞中。巨球蛋白介导转钴胺素-Cbl 复合物进入近端肾小管细胞的摄取。巨球蛋白参与 AGEs 的摄取和降解。在衰老、糖尿病或肾功能障碍时，AGEs 可能会使巨球蛋白超载，从而降低 Cbl 的摄取。转钴胺素-Cbl 可能会保留在血液中。在糖化条件下巨球蛋白和转钴胺素受体的脱落也是这种现象的可能机制。
