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Molecular and Cellular Biology, August 2000, p. 5840-5846, Vol. 20, No. 16
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Aldose Reductase-Deficient Mice Develop Nephrogenic Diabetes Insipidus

Horace T. B. Ho,1 Sookja K. Chung,1,* Janice W. S. Law,1 Ben C. B. Ko,1 Sidney C. F. Tam,2 Heddwen L. Brooks,3 Mark A. Knepper,3 and Stephen S. M. Chung1

Institute of Molecular Biology, The University of Hong Kong,1 and Division of Clinical Biochemistry, Queen Mary Hospital,2 Hong Kong, China, and Renal Mechanisms Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-16033

Received 16 March 2000/Accepted 11 May 2000

Aldose reductase (ALR2) is thought to be involved in the pathogenesis of various diseases associated with diabetes mellitus, such as cataract, retinopathy, neuropathy, and nephropathy. However, its physiological functions are not well understood. We developed mice deficient in this enzyme and found that they had no apparent developmental or reproductive abnormality except that they drank and urinated significantly more than their wild-type littermates. These ALR2-deficient mice exhibited a partially defective urine-concentrating ability, having a phenotype resembling that of nephrogenic diabetes insipidus.

* Corresponding author. Mailing address: Institute of Molecular Biology, South Wing, 8/F Kadoorie Biological Sciences Bldg., The University of Hong Kong, Pokfulam Rd., Hong Kong, China. Phone: (852) 2299-0783. Fax: (852) 2817-1006. E-mail: skchung{at}hkucc.hku.hk.

Molecular and Cellular Biology, August 2000, p. 5840-5846, Vol. 20, No. 16
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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