Mutant congenic strain
CSAL (Orléans) - 1981 (from The Jackson Laboratory in 1974)
Colour and related genotype:
Obese black mouse: Leprdb, related genotype: a/a, Leprdb/Leprdb
Non obese black mouse (control): Leprdb, Dock7m, related genotype: a/a, Leprdb/+, Dock7m/+
Non obese grey mouse (control): Dock7m, related genotype: a/a, Dock7m/Dock7m
Good breeder, mating scheme: heterozygous ♂ x heterozygous ♀ (the homozygous mice are steriles.)
Description of our model and application areas
The db mutation arose spontaneously in a colony of the inbred strain C57BL/Ks/J. This mutation was backcrossed by Coleman onto a C57/BL/6J background in order to maximize the expression of the mutant Leprdb gene. This leads to a compensatory hyperplasia of the β cells in the islets of Langerhans. This gene is located on chromosome 4. The Dock7m gene (dilution of coat colour) allows to identify WT individuals for the Lepr+ gene.
This strain is a model of Type II diabetes (NIDDM) and is used in hyperglycemia, hyperinsulinaemia, insulin resistance, obesity-related diabetes, diabetic complications. (delayed scar formation, fertility problems, peripheral neuropathy, cardiomyopathy…), and endocrine disease (defects of lipocytes, hypothalamus, pituitary gland and pancreas) studies.
Main application and research fields
Download the technical sheet
Health monitoring report
The growth curve represents an average which reflects the weight variation of the strain measured between 21 and 84 days for males and females.
Glucose and Insuline
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