Kodama H, Okada S, Inui K, Yutaka T, Yabuuchi H
Tohoku J Exp Med. 1980 Aug;131(4):347-53. doi: 10.1620/tjem.131.347.
Urinary excretion of the organic acids in patients with type I and III glycogenosis was investigated. In all patients with type I glycogenosis, urinary alpha-ketoglutarate concentration ws about 10 times the normal value. alpha-Ketoglutaric aciduria was not improved by the acute or prolonged administration of a large dose of factors for pyruvate- and alpha-ketoglutarate dehydrogenase complex. On the other hand, the level of alpha-ketoglutarate in the urine from type I patients decreased in conjunction with the decrease of plasma lactate and pyruvate concentration after repeated oral glucose loading. Oral citrate loading brought an increased excretion of alpha-ketoglutarate in type I glycogenosis. It is possible that alpha-ketoglutarate dehydrogenase in the rate-limiting step in tricarboxylic acid cycle and in patients with glycogenosis type I, the excessive excretion of alpha-ketoglutarate may be caused by the limited activity of alpha-ketoglutarate dehydrogenase with excessive substrate.
对I型和III型糖原贮积病患者的有机酸尿排泄情况进行了研究。在所有I型糖原贮积病患者中,尿中α-酮戊二酸浓度约为正常值的10倍。急性或长期大剂量给予丙酮酸和α-酮戊二酸脱氢酶复合物的相关因子后,α-酮戊二酸尿症并未改善。另一方面,I型患者尿液中α-酮戊二酸水平随着重复口服葡萄糖负荷后血浆乳酸和丙酮酸浓度的降低而下降。口服柠檬酸盐负荷使I型糖原贮积病患者的α-酮戊二酸排泄增加。三羧酸循环限速步骤中的α-酮戊二酸脱氢酶可能存在问题,在I型糖原贮积病患者中,α-酮戊二酸的过度排泄可能是由于底物过多时α-酮戊二酸脱氢酶活性受限所致。