Kishi T, Kishi H, Watanabe T, Folkers K
J Med. 1976;7(3-4):307-21.
The activity of the succinate dehydrogenase-coenzyme Q10 reductase from 120 diabetic patients was significantly lower (P less than 0.001) and the per cent deficiency was significantly higher (P less than 0.001) than that of the controls. The diabetes of 37 patients was controlled by diet; the enzyme activity was lower (P less than 0.001) and the deficiency was higher (P less than 0.02) than for controls. In decreasing effectiveness, Dymelor, Glyburide, Phenformin and Tolazamide inhibited the COQ10-enzyme, NADH-oxidase. Tolbutamide, Glypizide, and Chlorpropamide were noninhibitory to succinoxidase and NADH-oxidase. Patients receiving Tolazamide and Phenformin showed a higher incidence (P less than 0.001 to P less than 0.05) of COQ10-deficiency than patients controlled by diet or normal controls. Certain diabetic patients controlled by diet may have a deficiency of COQ10 which may be enhanced by the inhibition by certain commonly used antidiabetic drugs of COQ10-enzymes. A deficiency of COQ10 in the pancreas could impair bioenergetics, the generation of ATP, and the biosynthesis of insulin.
120名糖尿病患者的琥珀酸脱氢酶 - 辅酶Q10还原酶活性显著低于对照组(P < 0.001),缺乏率显著高于对照组(P < 0.001)。37名患者通过饮食控制糖尿病;其酶活性低于对照组(P < 0.001),缺乏率高于对照组(P < 0.02)。按抑制效果递减,甲磺丁脲、格列本脲、苯乙双胍和甲苯磺丁脲抑制辅酶Q10 - 酶、NADH - 氧化酶。甲苯磺丁脲、格列吡嗪和氯磺丙脲对琥珀酸氧化酶和NADH - 氧化酶无抑制作用。接受甲苯磺丁脲和苯乙双胍治疗的患者辅酶Q10缺乏的发生率高于饮食控制的患者或正常对照组(P < 0.001至P < 0.05)。某些通过饮食控制的糖尿病患者可能存在辅酶Q10缺乏,某些常用抗糖尿病药物对辅酶Q10 - 酶的抑制作用可能会加剧这种缺乏。胰腺中辅酶Q10缺乏可能损害生物能量学、ATP的生成以及胰岛素的生物合成。