Disruption of Aldose Reductase Gene (Akr1b1) Causes Defect in Urinary Concentrating Ability and Divalent Cation Homeostasis
| Autor: | Jing Chen, Kaoru Aida, Yukinobu Ikegishi, Sadahiro Ito, Toshimasa Onaya, Masato Tawata, Shuichiro Maeda |
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| Rok vydání: | 2000 |
| Předmět: |
Blood Glucose
Kidney Renal Agents Biochemistry Mice chemistry.chemical_compound Polyol pathway Deamino Arginine Vasopressin Magnesium Hypercalciuria Mice Knockout chemistry.chemical_classification Immunohistochemistry Blotting Southern Phenotype medicine.anatomical_structure Creatinine Hypermagnesemia medicine.medical_specialty Genotype Blotting Western Biophysics Phosphates Divalent Chlorides Aldehyde Reductase Cations Internal medicine medicine Animals Molecular Biology Gene Library Aldose reductase Models Genetic Water Deprivation Body Weight Sodium Water Cell Biology medicine.disease Mice Inbred C57BL Glucose Endocrinology chemistry Potassium Calcium Sorbitol Gene Deletion Homeostasis |
| Zdroj: | Biochemical and Biophysical Research Communications. 277:281-286 |
| ISSN: | 0006-291X |
| Popis: | 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 hypercalciuria, hypercalcemia, hypermagnesemia, and reduced ability to concentrate urine, suggesting a new physiological role of AKR1B1 in divalent cation homeostasis. |
| Databáze: | OpenAIRE |
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