Prevention of urinary albumin excretion in 6 month streptozocin-diabetic rats with the aldose reductase inhibitor tolrestat

1988 ◽  
Vol 2 (1) ◽  
pp. 16-18 ◽  
Author(s):  
Michael L. McCaleb ◽  
Janet Sredy ◽  
Jane Millen ◽  
Denis M. Ackerman ◽  
Dushan Dvornik
Nephron ◽  
1998 ◽  
Vol 80 (3) ◽  
pp. 277-284 ◽  
Author(s):  
Aileen V. McAuliffe ◽  
Belinda A. Brooks ◽  
Elizabeth J. Fisher ◽  
Lynda M. Molyneaux ◽  
Dennis K. Yue

1997 ◽  
Vol 272 (5) ◽  
pp. E918-E924 ◽  
Author(s):  
H. Gronbaek ◽  
P. Volmers ◽  
S. F. Bjorn ◽  
R. Osterby ◽  
H. Orskov ◽  
...  

Growth hormone (GH) and insulin-like growth factor I (IGF-I) may play a role in early diabetic renal and glomerular growth and in the later development of experimental diabetic kidney disease. Rats from a genetic GH/IGF-I-deficient dwarf rat strain were made streptozotocin diabetic and were compared with nondiabetic dwarf rats. GH/IGF-I-intact rats with and without diabetes served as controls. After 6 mo of diabetes, kidney weight and total glomerular volume increased significantly in GH/IGF-I-intact diabetic rats compared with the nondiabetic GH/IGF-I-intact rats (P < 0.05), whereas the diabetic dwarf rats had insignificant changes compared with dwarf control rats. By the end of the study, urinary albumin excretion (UAE) increased from similar base levels of approximately 15-20 micrograms/24 h to 473 +/- 52 (SE) micrograms/24 h in GH/IGF-I-intact diabetic rats compared with 151 +/- 32 micrograms/24 h in diabetic dwarf rats (P < 0.01). In conclusion, isolated GH/IGF-I deficiency reduces the degree of renal and glomerular hypertrophy and the increase in UAE after 6 mo of experimental diabetes in GH/IGF-I-deficient rats.


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