BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ

These double mutant mice harbor both the Leprdb spontaneous mutation and the Nos3 (eNOS) targeted mutation and are congenic on C57BLKS/J genetic background. Mice homozygous for both mutations (called eNOS-/- C57BLKS/J db/db, eNOS-/- db/db, or db/db/eNOS-/- double mutant mice) are viable with development of type II diabetes and diabetic nephropathy. The eNOS-/- C57BLKS/J db/db mice develop type II diabetes with significant obesity and hypertension: while both mutations are associated with insulin resistance, the mutated leptin receptor in db/db mice chiefly accounts for the observed hyperglycemia and defective leptin signaling (leading to persistent hyperphagia and obesity), and the eNOS-deficiency accounts for the moderate systemic hypertension. In addition, eNOS-/- C57BLKS/J db/db mice exhibit rapid onset and progression of pathologic diabetic nephropathy (DN) features by 26 weeks of age; developing severe albuminuria and other DN characteristics (including arteriolar hyalinosis, increased glomerular basement membrane thickness, mesangial expansion, mesangiolysis, and focal segmental and early nodular glomerulosclerosis), also with remarkably decreased glomerular filtration rate (GFR; on the basis of impaired inulin clearance and increased serum creatinine). Double homozygous eNOS-/- C57BLKS/J db/db mice are a robust model of type II diabetic nephropathy and may be useful for studying eNOS-mediated events in the development and progression of diabetic nephropathy.

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Data (.csv filetype)

W rodent (g)

BKS.Cg-Leprdb Nos3tm1Unc/RhrsJBoth755.193.07
Avg = 55.19
Std = 3.07
N = 7

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