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关于实验性糖尿病胰岛素治疗相关钠潴留的观察

Observations on sodium retention related to insulin treatment of experimental diabetes.

作者信息

Blumenthal S A

出版信息

Diabetes. 1975 Jul;24(7):645-9. doi: 10.2337/diab.24.7.645.

Abstract

Streptozotocin (STZ)-diabetic rats regularly retained sodium (Na+), and tended to retain potassium (K+) as well, in response to insulin. Diabetic patients have also been reported to exhibit antinatriuresis and antikaliuresis early in the course of insulin therapy. Insulin-related Na+ retention can occur without a marked reduction in blood glucose level and does not appear to be attributable to preexisting Na+ depletion, mineralocorticoid effect, or suppression of glucosuria. The decrease in urinary Na+ excretion (UNaV) in the rats incident to insulin administration was appreciably greater than the decrease in chloride (Cl-) or water excretion. The significance of this observation is uncertain. It may be, in part, a consequence of the nephrotoxicity of STZ. Insulin-related Na+ retention may be closely related pathogenetically to the Na+ retention of refeeding and may reflect a direct renal action of insulin or, less likely, an alteration of renal tubular metabolism in response to insulin-mediated changes in sytemic metabolism.

摘要

链脲佐菌素(STZ)诱导的糖尿病大鼠在注射胰岛素后会规律性地潴留钠(Na+),并且也倾向于潴留钾(K+)。据报道,糖尿病患者在胰岛素治疗早期也会出现钠排泄减少和钾排泄减少。胰岛素相关的钠潴留可在血糖水平无明显降低的情况下发生,且似乎并非由先前存在的钠缺乏、盐皮质激素作用或糖尿抑制所致。给大鼠注射胰岛素后,尿钠排泄量(UNaV)的减少明显大于氯(Cl-)或水排泄量的减少。这一观察结果的意义尚不确定。这可能部分是链脲佐菌素肾毒性的结果。胰岛素相关的钠潴留可能在发病机制上与再喂养时的钠潴留密切相关,可能反映了胰岛素对肾脏的直接作用,或者可能性较小的是,肾小管代谢因胰岛素介导的全身代谢变化而发生改变。

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