Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age with elevations of plasma insulin beginning at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric.Read More +
In the spring of 2009, The Jackson Laboratory eliminated the allele misty (m) from the 000697 colony. Misty was bred out at generation 86. It is distributed as B6.D2(BKS)-Dock7m/J (009659).
Mice homozygous for the diabetes spontaneous mutation (Leprdb) become identifiably obese around 3 to 4 weeks of age. Elevations of plasma insulin begin at 10 to 14 days and of blood sugar at four to eight weeks. Affected mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. On the C57BL/6 background there is compensatory hyperplasia of the islet B cells, and continued hyperinsulinemia throughout an 18- to 20-month life span. Wound healing is delayed and metabolic efficiency is increased. Although normal in body weight, blood glucose, and plasma insulin, heterozygotes (Leprdb/+) also have increased metabolic efficiency and can survive a prolonged fast longer than controls. Experiments involving destruction of the ventromedial nucleus of the hypothalamus suggest that Leprdb may cause a defect in the hypothalamus. Steroid sulfotransferase enzymes, aberrantly expressed in diabetic mice, interact with the Leprdb mutation as modifiers of gender differences in obesity-induced diabetes susceptibility.
For Heterozygous mice only, this strain ships with a JAXTagTM affixed. Learn more about JAXTagTM.
The spontaneous autosomal recessive mutation diabetes, db was discovered at The Jackson Laboratory, Bar Harbor, ME in 1966 on the inbred strain C57BLKS/J. Formerly known as db, after cloning it became Leprdb. Additional backgrounds available: C57BLKS/J-Dock7m +/+ Leprdb (000642), C57BL/6J-Dock7m Leprdb/+ + (000699), C57BLKS/J-Dock7m Leprdb/+ + (000700).
|Allele Synonym(s)||db; db/db; Lepdb; Lepr-; Leprdb-1J; leprdb|
|Gene Symbol and Name||Lepr, leptin receptor|
|Strain of Origin||C57BLKS/J|
|General Note|| |
Phenotypic Similarity to Human Syndrome: Gestational Diabetes J:219658
|Molecular Note||An intronic G-to-T transversion in this allele created a donor splice site that causes abnormal splicing and the inclusion of 106 nt of intronic sequence in the transcript, leading to premature termination of the long cellular domain of the Ob-Rb splice form and loss of its signal transducing function.|
When maintaining a live colony, these mice are bred as heterozygotes. Females homozygous for the mutation are infertile and males exhibit a reduced ability to mate.
Wean-aged mice may show signs of barbering that include whisker picking. Affected mice typically regrow whiskers within two weeks after weaning.
When using the B6 db mouse strain in a publication, please cite the originating article(s) and include JAX stock #000697 in your Materials and Methods section.
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