Genetic deficiency of aldose reductase counteracts the development of diabetic nephropathy in C57BL/6 mice.

ABSTRACT:

Aims/hypothesis

The aim of the study was to investigate the effects of genetic deficiency of aldose reductase in mice on the development of key endpoints of diabetic nephropathy.

Methods

A line of Ar (also known as Akr1b3)-knockout (KO) mice, a line of Ar-bitransgenic mice and control C57BL/6 mice were used in the study. The KO and bitransgenic mice were deficient for Ar in the renal glomeruli and all other tissues, with the exception of, in the bitransgenic mice, a human AR cDNA knockin-transgene that directed collecting-tubule epithelial-cell-specific AR expression. Diabetes was induced in 8-week-old male mice with streptozotocin. Mice were further maintained for 17 weeks then killed. A number of serum and urinary variables were determined for these 25-week-old mice. Perio

SUBMITTER: Liu H 

PROVIDER: S-EPMC3071933 | biostudies-literature | 2011 May

REPOSITORIES: biostudies-literature