Ahloulay M, Schmitt F, Déchaux M, Bankir L
INSERM Unité 367, Institut du Fer à Moulin, Paris, France.
Diabetes Metab. 1999 Sep;25(3):213-22.
In diabetes mellitus (DM), the high urine flow rate suggests that urinary concentrating capacity is impaired. However, several studies have shown that vasopressin is elevated in DM and the consequences of this elevation have not yet been characterized. This study reevaluated renal function and water handling in male Wistar rats with Streptozotocin-induced DM, and in control rats. During five weeks after induction of DM, urine was collected in metabolic cages and a blood sample was drawn during the third week. Control rats (CONT) were studied in parallel. On week 3, urine flow rate was tenfold higher in DM than in CONT rats and urinary osmolality was reduced by half along with a markedly higher osmolar excretion (DM/CONT = 5.87), due for a large part to glucose but also to urea (DM/CONT = 2.49). Glucose represented 52% of total osmoles (90.3 +/- 6.5 mmol/d out of 172 +/- 14 mosm/d). Free water reabsorption was markedly higher in DM rats compared to CONT (326 +/- 24 vs 81 +/- 5 ml/d). In other rats treated in the same way, urinary excretion of vasopressin was found to be markedly elevated (15.1 +/- 4.1 vs 1.44 +/- 0.23 ng/d). In DM rats, glucose concentration in urine was 17 fold higher than in plasma, and urea concentration 14 fold higher. Both urine flow rate and free water reabsorption were positively correlated with the sum of glucose and urea excretions (r = 0.967 and 0.653, respectively) thus demonstrating that the urinary concentrating activity of the kidney increased in proportion to the increased load of these two organic solutes. These results suggest that vasopressin elevation in DM contributes to increase urinary concentrating activity and thus to limit water requirements induced by the metabolic derangements of DM. The possible deleterious consequences of sustained high level of vasopressin in DM are discussed.
在糖尿病（DM）中，高尿流率表明尿浓缩能力受损。然而，多项研究表明，糖尿病患者体内抗利尿激素水平升高，但其升高的后果尚未明确。本研究重新评估了链脲佐菌素诱导的糖尿病雄性Wistar大鼠及对照大鼠的肾功能和水代谢情况。在诱导糖尿病后的五周内，将大鼠置于代谢笼中收集尿液，并在第三周采集血样。同时对对照大鼠（CONT）进行平行研究。在第3周时，糖尿病大鼠的尿流率比对照大鼠高10倍，尿渗透压降低一半，同时渗透压排泄显著增加（糖尿病组/对照组 = 5.87），这在很大程度上归因于葡萄糖，但也与尿素有关（糖尿病组/对照组 = 2.49）。葡萄糖占总渗透摩尔数的52%（172 ± 14 mosm/d中的90.3 ± 6.5 mmol/d）。与对照大鼠相比，糖尿病大鼠的自由水重吸收显著更高（326 ± 24 vs 81 ± 5 ml/d）。在以相同方式处理的其他大鼠中，发现抗利尿激素的尿排泄显著升高（15.1 ± 4.1 vs 1.44 ± 0.23 ng/d）。在糖尿病大鼠中，尿中葡萄糖浓度比血浆高17倍，尿素浓度高14倍。尿流率和自由水重吸收均与葡萄糖和尿素排泄量之和呈正相关（r分别为0.967和0.653），从而表明肾脏的尿浓缩活性与这两种有机溶质负荷的增加成比例增加。这些结果表明，糖尿病患者抗利尿激素水平升高有助于增加尿浓缩活性，从而限制糖尿病代谢紊乱引起的水分需求。本文还讨论了糖尿病患者抗利尿激素持续高水平可能产生的有害后果。
