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肾刷状缘小泡中的肌醇转运及其被D-葡萄糖抑制的情况。

myo-Inositol transport in renal brush border vesicles and it inhibition by D-glucose.

作者信息

Hammerman M R, Sacktor B, Daughaday W H

出版信息

Am J Physiol. 1980 Aug;239(2):F113-20. doi: 10.1152/ajprenal.1980.239.2.F113.

DOI:10.1152/ajprenal.1980.239.2.F113
PMID:6773422
Abstract

We examined the mechanism of myo-inositol uptake by rabbit renal proximal tubule brush border membrane vesicles and characterized the relationship between the transports of myo-inositol and D-glucose. A 100 mM Na+ electrochemical gradient (extravesicular medium > intravesicular medium) stimulated the initial rate of myo-inositol uptake 20- to 60-fold. Other cation gradients were ineffective. The Na+ myo-inositol co-transport system was shown to be electrogenic. The Na+ electrochemical gradient-dependent uptake of myo-inositol saturated at about 1 mM myo-inositol, with an apparent Km of 94 micro M at an initial 100 mM Na+ gradient. D-Glucose was an inhibitor of the Na+ gradient-dependent uptake of myo-inositol. D-Glucose, but not L-glucose, elicited accelerative exchange diffusion of myo-inositol. myo-Inositol did not significantly inhibit the Na+ gradient-dependent transport of D-glucose. We suggest that D-glucose inhibits myo-inositol uptake by dissipating the membrane potential and sharing the myo-inositol carrier. The inhibition of myo-inositol transport across the brush border membrane by D-glucose explains how glycosuria could produce inosituria in patients with diabetes mellitus.

摘要

我们研究了兔肾近端小管刷状缘膜囊泡摄取肌醇的机制,并对肌醇与D-葡萄糖转运之间的关系进行了表征。100 mM的Na⁺电化学梯度(囊泡外介质>囊泡内介质)使肌醇摄取的初始速率提高了20至60倍。其他阳离子梯度无效。Na⁺-肌醇共转运系统显示为电生性的。在初始100 mM Na⁺梯度下,依赖Na⁺电化学梯度的肌醇摄取在约1 mM肌醇时达到饱和,表观Km为94 μM。D-葡萄糖是Na⁺梯度依赖性肌醇摄取的抑制剂。D-葡萄糖而非L-葡萄糖引发了肌醇的加速交换扩散。肌醇并未显著抑制Na⁺梯度依赖性的D-葡萄糖转运。我们认为,D-葡萄糖通过耗散膜电位和共用肌醇载体来抑制肌醇摄取。D-葡萄糖对肌醇跨刷状缘膜转运的抑制解释了糖尿病患者中糖尿如何导致肌醇尿。

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