首页> 外文期刊>American Journal of Physiology >Gene deletion of the Na~+-glucose cotransporter SGLT1 ameliorates kidney recovery in a murine model of acute kidney injury induced by ischemia-reperfusion
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Gene deletion of the Na~+-glucose cotransporter SGLT1 ameliorates kidney recovery in a murine model of acute kidney injury induced by ischemia-reperfusion

机译:Na~+-葡萄糖协同转运蛋白SGLT1的基因缺失改善了缺血再灌注诱导的急性肾损伤小鼠模型中的肾脏恢复

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摘要

Absence of SGLT1 did not affect the initial kidney impairment versus WT mice, as indicated by similar increases on day 1 in plasma concentrations of creatinine and urinary excretion of the tubular injury marker kidney injury molecule-1 as well as a similar rise in plasma osmolality and fall in urine osmolality as indicators of impaired urine concentration. Recovery of kidney function on days 14/16, however, was improved in Sgltl ' versus WT mice, as indicated by lower plasma creatinine, higher glomerula filtration rate (by FITC-sinistrin in awake mice), and more completely restored urine and plasma osmolality.
机译:与WT小鼠相比,SGLT1的缺失并不影响初始肾损伤,如第1天血浆肌酐浓度和肾小管损伤标志物肾损伤分子-1的尿排泄量增加,以及血浆渗透压的类似升高和尿渗透压下降作为尿液浓度受损的指标。然而,与WT小鼠相比,Sgltl小鼠在第14/16天的肾功能恢复有所改善,如血浆肌酐降低,肾小球滤过率较高(清醒小鼠中的FITC-sinistrin)以及更完全恢复的尿液和血浆渗透压所示。

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