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遗传性糖尿病小鼠中胆碱乙酰转移酶和6-磷酸果糖激酶活性的轴突运输

Axonal transport of choline acetyltransferase and 6-phosphofructokinase activities in genetically diabetic mice.

作者信息

Calcutt N A, Willars G B, Tomlinson D R

机构信息

Department of Physiology and Pharmacology, Medical School, University of Nottingham, UK.

出版信息

Muscle Nerve. 1988 Dec;11(12):1206-10. doi: 10.1002/mus.880111204.

DOI:10.1002/mus.880111204
PMID:2467203
Abstract

This study examined the anterograde axonal transport of activities of the cytoplasmic enzymes choline acetyltransferase and 6-phosphofructokinase in genetically diabetic C57BL/Ks (db/db) mice and their nondiabetic (+/?) littermates. Diabetic mice exhibited marked reductions in the accumulation of both choline acetyltransferase and 6-phosphofructokinase activity against a constriction of the left sciatic nerve (38% and 51% of nondiabetic values, respectively). Enzyme activities per unit length of unconstricted nerve were not different from those of nondiabetic mice. The nerves of diabetic mice did not accumulate measurable amounts of sorbitol or fructose and showed no myo-inositol depletion. Thus this study concludes that, in diabetic mice, the deficits in anterograde axonal transport of these two enzymes do not arise from the accumulation of sorbitol and fructose nor from depletion of nerve free myo-inositol.

摘要

本研究检测了遗传性糖尿病C57BL/Ks(db/db)小鼠及其非糖尿病(+/?)同窝仔鼠中细胞质酶胆碱乙酰转移酶和6-磷酸果糖激酶活性的顺行轴突运输情况。糖尿病小鼠在左侧坐骨神经受压后,胆碱乙酰转移酶和6-磷酸果糖激酶活性的积累均显著降低(分别为非糖尿病小鼠值的38%和51%)。未受压神经单位长度的酶活性与非糖尿病小鼠无异。糖尿病小鼠的神经未积累可测量量的山梨醇或果糖,且未出现肌醇耗竭。因此,本研究得出结论,在糖尿病小鼠中,这两种酶顺行轴突运输的缺陷并非由山梨醇和果糖的积累或神经游离肌醇的耗竭引起。

相似文献

1
Axonal transport of choline acetyltransferase and 6-phosphofructokinase activities in genetically diabetic mice.遗传性糖尿病小鼠中胆碱乙酰转移酶和6-磷酸果糖激酶活性的轴突运输
Muscle Nerve. 1988 Dec;11(12):1206-10. doi: 10.1002/mus.880111204.
2
Axonal transport and nerve conduction and their relation to nerve polyol and myo-inositol levels in spontaneously diabetic BB/D rats.自发性糖尿病BB/D大鼠的轴突运输、神经传导及其与神经多元醇和肌醇水平的关系。
Neurochem Pathol. 1984;2(4):285-93.
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Defects of axonal transport in experimental diabetes that are unrelated to the sorbitol pathway.实验性糖尿病中与山梨醇途径无关的轴突运输缺陷。
Exp Neurol. 1987 Apr;96(1):194-202. doi: 10.1016/0014-4886(87)90180-4.
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Reversal of deficits in axonal transport and nerve conduction velocity by treatment of streptozotocin-diabetic rats with myo-inositol.用肌醇治疗链脲佐菌素诱导的糖尿病大鼠可逆转轴突运输和神经传导速度的缺陷。
Exp Neurol. 1985 Aug;89(2):420-7. doi: 10.1016/0014-4886(85)90101-3.
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Ganglioside treatment of streptozotocin-diabetic rats prevents defective axonal transport of 6-phosphofructokinase activity.用神经节苷脂治疗链脲佐菌素诱导的糖尿病大鼠可预防6-磷酸果糖激酶活性的轴突运输缺陷。
J Neurochem. 1988 May;50(5):1478-83. doi: 10.1111/j.1471-4159.1988.tb03033.x.
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Reduced anterograde and retrograde accumulation of axonally transported phosphofructokinase in streptozotocin-diabetic rats: effects of insulin and the aldose reductase inhibitor 'Statil'.链脲佐菌素诱导的糖尿病大鼠轴突运输磷酸果糖激酶的顺行和逆行积累减少:胰岛素和醛糖还原酶抑制剂“Statil”的作用
Diabetologia. 1987 Apr;30(4):239-43. doi: 10.1007/BF00270422.
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Prevention of defects of axonal transport in experimental diabetes by aldose reductase inhibitors.醛糖还原酶抑制剂对实验性糖尿病轴突运输缺陷的预防作用。
Drugs. 1986;32 Suppl 2:15-8. doi: 10.2165/00003495-198600322-00005.
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Effects of sorbitol dehydrogenase deficiency on nerve conduction in experimental diabetic mice.山梨醇脱氢酶缺乏对实验性糖尿病小鼠神经传导的影响。
Diabetes. 1998 Jun;47(6):961-6. doi: 10.2337/diabetes.47.6.961.
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Prevention of defective axonal transport in streptozocin-diabetic rats by treatment with "Statil" (ICI 128436), an aldose reductase inhibitor.用醛糖还原酶抑制剂“Statil”(ICI 128436)治疗可预防链脲佐菌素诱导的糖尿病大鼠轴突运输缺陷。
Diabetes. 1985 Oct;34(10):970-2. doi: 10.2337/diab.34.10.970.
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Streptozotocin-induced diabetes causes metabolic changes and alterations in neurotrophin content and retrograde transport in the cervical vagus nerve.链脲佐菌素诱导的糖尿病会导致代谢变化以及颈迷走神经中神经营养因子含量和逆行运输的改变。
Exp Neurol. 2001 Jul;170(1):149-61. doi: 10.1006/exnr.2001.7673.

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