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肌醇补充剂对科恩糖尿病(2型)大鼠肾脏病理变化发展的影响。

Effect of myo-inositol supplementation on the development of renal pathological changes in the Cohen diabetic (type 2) rat.

作者信息

Cohen A M, Wald H, Popovtzer M, Rosenmann E

机构信息

Department of Pathology, Hadassah Hebrew University Hospital, Jerusalem, Israel.

出版信息

Diabetologia. 1995 Aug;38(8):899-905. doi: 10.1007/BF00400577.

DOI:10.1007/BF00400577
PMID:7589874
Abstract

A lower concentration of intracellular myo-inositol has been implicated in the development of diabetic nephropathy. This was based on short-term studies showing that early administration of aldose reductase inhibitors or myo-inositol supplementation reduces increased glomerular filtration rate and partly reduces increased urinary albumin excretion in streptozotocin diabetic rats. We studied the effect of long-term (4 months) administration of 1% myo-inositol supplement to the Cohen diabetic (type 2) rat on the development of nephropathy and renal Na(+)-K(+)-ATPase. This treatment reduced the increased renal Na(+)-K(+)-ATPase activity but had no effect on blood glucose levels, body weight, increased kidney weight, or creatinine clearance and did not prevent or reduce the development of renal glomerular pathology. There was no correlation between the level of Na(+)-K(+)-ATPase activity and the degree of nephropathy. It is possible that the renal pathological changes are due to metabolic and humoral factors resulting from hyperglycaemia, other than myo-inositol depletion. The fact that myo-inositol treatment had no effect on the development of renal pathological changes but was shown to have a beneficial effect on restoring impaired conduction velocity and on the disruption of structural elements in the nerve indicates that the effect of the biological changes ensuing from hyperglycaemia vary in different tissues depending on local conditions.

摘要

细胞内肌醇浓度降低与糖尿病肾病的发生有关。这是基于短期研究得出的结论,这些研究表明,早期给予醛糖还原酶抑制剂或补充肌醇可降低链脲佐菌素诱导的糖尿病大鼠肾小球滤过率的升高,并部分降低尿白蛋白排泄量的增加。我们研究了对科恩糖尿病(2型)大鼠长期(4个月)给予1%肌醇补充剂对肾病发展和肾钠钾ATP酶的影响。这种治疗降低了肾钠钾ATP酶活性的升高,但对血糖水平、体重、肾脏重量增加或肌酐清除率没有影响,也不能预防或减少肾小球病理改变的发展。钠钾ATP酶活性水平与肾病程度之间没有相关性。肾脏病理变化可能是由高血糖导致的代谢和体液因素引起的,而非肌醇缺乏。肌醇治疗对肾脏病理变化的发展没有影响,但对恢复受损的神经传导速度和神经结构成分的破坏有有益作用,这一事实表明,高血糖引起的生物学变化在不同组织中的影响因局部条件而异。

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肌醇在疾病与发育中的作用:-肌醇加氧酶代谢途径的角色
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