Sebeková K, Spustová V, Dzúrik R
Clinic of Pharmacotherapy, Institute of Preventive and Clinical Medicine, Bratislava, Slovakia.
Int Urol Nephrol. 1996;28(1):123-31. doi: 10.1007/BF02550149.
Accumulated end-products were identified to participate in the late development of glucose intolerance and insulin resistance (IR) in patients with chronic renal insufficiency. The possible pathophysiological role of accumulated 5-hydroxy-indoleacetic acid (5HIAA) in the genesis of IR was investigated employing an in vitro animal model. 5HIAA inhibited the basal glucose uptake in isolated rat soleus muscle with intact membrane with A50 = 1.25 mumol/l, and Emax = 88.6%. 5HIAA significantly inhibited the insulin, and tolbutamide stimulated glucose uptake. In Ca and Mg depletion 5HIAA showed a partially additive inhibitory effect, while nonadditive inhibitory activity was observed in the case of K+ excess. It is concluded that 5HIAA is a metabolically active end-product interfering with glucose uptake in muscle at an insulin postreceptor level, and its effect is related to Ca modulation in the insulin regulatory cascade.
已确定累积的终产物参与慢性肾功能不全患者糖耐量异常和胰岛素抵抗（IR）的后期发展。采用体外动物模型研究了累积的5-羟色胺酸（5HIAA）在IR发生中的可能病理生理作用。5HIAA抑制完整膜的离体大鼠比目鱼肌基础葡萄糖摄取，A50 = 1.25 μmol/l，Emax = 88.6%。5HIAA显著抑制胰岛素和甲苯磺丁脲刺激的葡萄糖摄取。在钙和镁缺乏时，5HIAA表现出部分相加抑制作用，而在钾过量时观察到非相加抑制活性。结论是，5HIAA是一种代谢活性终产物，在胰岛素受体后水平干扰肌肉中的葡萄糖摄取，其作用与胰岛素调节级联中的钙调节有关。
