| Authors |
Qi Z, Fujita H, Jin J, Davis LS, Wang Y, Fogo AB, Breyer MD
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| Submitted By |
Matthew Breyer on 11/12/2007 |
| Status |
Published |
| Journal |
Diabetes |
| Year |
2005 |
| Date Published |
9/1/2005 |
| Volume : Pages |
54 : 2628 - 2637 |
| PubMed Reference |
16123351 |
| Abstract |
Differential susceptibility to diabetic nephropathy has been observed in humans,
but it has not been well defined in inbred strains of mice. The present studies
characterized the severity of diabetic nephropathy in six inbred mouse strains
including C57BL/6J, DBA/2J, FVB/NJ, MRL/MpJ, A/J, and KK/HlJ mice. Diabetes
mellitus was induced using low-dose streptozotocin injection. Progression of
renal injury was evaluated by serial measurements of urinary albumin excretion,
glomerular filtration rate (GFR), and terminal assessment of renal morphology
over 25 weeks. Despite comparable levels of hyperglycemia, urinary albumin
excretion and renal histopathological changes were dramatically different among
strains. DBA/2J and KK/HlJ mice developed significantly more albuminuria than
C57BL/6J, MRL/MpJ, and A/J mice. Severe glomerular mesangial expansion, nodular
glomerulosclerosis, and arteriolar hyalinosis were observed in diabetic DBA/2J
and KK/HlJ mice. Glomerular hyperfiltration was observed in all diabetic strains
studied except A/J. The significant decline in GFR was not evident over the
25-week period of study, but diabetic DBA/2J mice exhibited a tendency for GFR
to decline. Taken together, these results indicate that differential
susceptibility to diabetic nephropathy exists in inbred mice. DBA/2J and KK/HlJ
mice are more prone to diabetic nephropathy, whereas the most widely used
C57BL/6J mice are relatively resistant to development of diabetic nephropathy.
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