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Diabetic (db/db) mice

Characteristics / Husbandry

  • Coat: Black or misty
  • Leprdb is an autosomal-recessive mutation on chromosome 4
  • Obesity expressed at 4-5 weeks of age
  • Elevation of plasma insulin demonstrated at 10-14 days
  • Polyphagia
  • Proteinuria
  • Glycosuria
  • Polyuria/Polydipsia
  • Hyperinsulinemia despite severe depletion of pancreatic islet insulin-producing B-cells
  • Leptin receptor deficient
  • Hyperglycemia develops at 4-8 weeks of age
Immunology
Diabetes Type 2
General Studies
Myocardian Disease
Metabolism
Obesity
Obesity
Immunology
Diabetes, Type 2
Peripheral neuropathy
Myocardial disease
Immunodeficiency
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Reaching your goals in diabetes and obesity studies can be a challenge or a success depending on the reliability of your research models. The Leprdb mutation was discovered in 1966 in the inbred BKS mouse strain. This model has since been well characterized as a model of Type 2 diabetes mellitus, exhibiting commonly published metabolic symptoms including hyperglycemia and hyperinsulinemia.

From Dunn Nutritional Laboratory, Cambridge, United Kingdom; to Olac, United Kingdom, in 1979; to Harlan, United States in 2000. Harlan became Envigo in 2015.

Our breeding scheme maintains Dock7m and Leprdb in repulsion. These genes are closely linked; however, recombination could occur. Our mice are most likely nonrecombinants, but they have not been tested.

Order Code: 173(db)/174(lean)

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