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Mouse Models of Diabetic Nephropathy

Matthew D. Breyer, Erwin Böttinger, Frank C. Brosius, Thomas M. Coffman, Raymond C. Harris, Charles W. Heilig, Kumar Sharma and ; for the AMDCC
JASN January 2005, 16 (1) 27-45; DOI: https://doi.org/10.1681/ASN.2004080648
Matthew D. Breyer
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Erwin Böttinger
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Frank C. Brosius III
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Thomas M. Coffman
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Raymond C. Harris
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Charles W. Heilig
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Kumar Sharma
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    Figure 1.

    Summary of studies in the literature examining 24-h albumin excretion in mouse models of diabetes (#, reference number). For each study, a pair of bars represent mean ± SE. On the left, 24-hr albumin excretion in the diabetic cohort; on the right, the nondiabetic cohort. From left to right are albuminuria in C57BL/6 mice treated with multiple low-dose streptozotocin (STZ); C57BL6 high-dose STZ; C57BL6 db/db mice, a model of type 2 diabetes; four studies measuring albuminuria in the C57BLKS db/db strain show generally higher albuminuria; a single study examining 24-h albuminuria in the KK-Ay strain shows robust albuminuria.

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    Table 1.

    Some mouse models of diabetes studied for diabetic nephropathya

    Mouse Model (Reference No.)Strains Reported (Reference No.)DiabeticTypeAdvantagesDisadvantages
    Streptozotocin (71,81,146,228–232)C57BL/6J, C57BLKS, Balb/c, ICR, DBA2, ROPType 1Well established, reproducible timing; may be established in strains both resistant and susceptible to DNPotential for nonspecific toxicity; strain-dependent dosing necessary; biohazard: potential mutagen
    Encephalomyocarditis virus D variant (153,233,234)DBA, Balb-CType 1May reproduce viral causes of type 1 diabetes in humans; DBA may be prone to DNPotential for nonspecific renal effects; strain-dependent dosing necessary; biohazard; not widely studied; renal functional effects not characterized
    Ins2 Akita (84,88,89)C57BL/6, C3HType 1Commercially available (JAX); autosomal dominant mutationPresently only C57BL/6 commercially available; C57BL/6 relatively resistant to nephropathy; hyper-glycemia in females is mild
    NOD (101,102,235,236)Inbred line derived from ICR (outbred line)Type 1Spontaneous development of β-cell failure may mimic pathophysiology of disease in humans (99); commercially availableUnpredictable timing of development of diabetes; no appropriate control strain; needs insulin therapy to survive long periods; multigenic-cause diabetes precludes easy intercrosses
    Db/db (22,134)C57BL/6, C57BLKS, DBA, FVB (129), CBA (237)Type 2Available on multiple strains; commercially availableInfertile; autosomal recessive; mutation in leptin receptor is a very rare cause of obesity and type 2 diabetes in humans
    Ob/ob (21)C57BL/6 (238), FVB/N (238), DBA2 (239,240)Type 2Exists on diverse inbred strains; nephropathy uncharacterized; commercially availableInfertility—can be circumvented with leptin; autosomal recessive; nephropathy uncharacterized; mutation of leptin is a very rare cause of obesity and type 2 diabetes in humans
    Agouti (Ay)KK (170,241,242), C57BL (243), C3H (243), FVB (244)Type 2KK strain is susceptible to renal injury with significant albuminuria; autosomal dominant; commercially availableHyperglycemia moderate in males more than in females; onset of diabetes is not well defined; nephropathy may not be robust in strains other than KK
    High-fat diet (112)C57BL/6 is main susceptible strain (245)Type 2Onset can be determined by the investigatorOnly C57BL/6 reported as susceptible; hyperglycemia not prominent
    • ↵a DN, diabetic nephropathy.

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Journal of the American Society of Nephrology: 16 (1)
Journal of the American Society of Nephrology
Vol. 16, Issue 1
1 Jan 2005
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Mouse Models of Diabetic Nephropathy
Matthew D. Breyer, Erwin Böttinger, Frank C. Brosius, Thomas M. Coffman, Raymond C. Harris, Charles W. Heilig, Kumar Sharma
JASN Jan 2005, 16 (1) 27-45; DOI: 10.1681/ASN.2004080648

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Mouse Models of Diabetic Nephropathy
Matthew D. Breyer, Erwin Böttinger, Frank C. Brosius, Thomas M. Coffman, Raymond C. Harris, Charles W. Heilig, Kumar Sharma
JASN Jan 2005, 16 (1) 27-45; DOI: 10.1681/ASN.2004080648
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  • Article
    • Abstract
    • Working Definition of DN
    • Characterization of DN in Mice
    • Assessment of Hyperglycemia in Mice
    • Assessment of Renal Function in Mice
    • Models of Type 1 Diabetes
    • Mouse Models of Type 2 Diabetes
    • Inbred Mice: Strain Dependence of DN
    • Monogenic Mutations and Transgenic Mice
    • Conclusions
    • Acknowledgments
    • References
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