Disruption of aldose reductase gene (Akr1b1) causes defect in urinary concentrating ability and divalent cation homeostasis

被引：32

作者：

Aida, K

Ikegishi, Y

Chen, J

Tawata, M

Ito, S

Maeda, S

Onaya, T ^{[1
]}

机构：

[1] Yamanashi Med Univ, Dept Internal Med 3, Yamanashi 4093898, Japan

[2] Yamanashi Med Univ, Dept Biochem 1, Yamanashi 4093898, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2000年 / 277卷 / 02期

关键词：

aldose reductase; AKR1B1; gene targeting; hypercalcemia; hypercalciuria; urinary concentrating ability; divalent cation homeostasis;

D O I：

10.1006/bbrc.2000.3648

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Aldose reductase (AKR1B1) is the first enzyme in the polyol pathway through which glucose is converted to sorbitol, and has been implicated in the etiology of diabetic complications. However, its physiological role is still not well understood. In the kidney, AKR1B1 is quite abundant in the collecting tubule cells and thought to provide protection against hypertonic environment. We report here that the mice lacking AKR1B1 showed hypercalcemia, hypercalcemia, hypermagnesemia, and reduced ability to concentrate urine, suggesting a new physiological role of AKR1B1 in divalent cation homeostasis. (C) 2000 Academic Press.

引用

页码：281 / 286

页数：6

共 19 条

[1] Induction of rat aldose reductase gene transcription is mediated through the cis-element, osmotic response element (ORE):: Increased synthesis and/or activation by phosphorylation of ORE-binding protein is a key step [J].