These mice carry a spontaneous mutation at the Lepr locus on a C57BL/6J background and are characterized by compensatory hyperplasia of the islet B-cells and hyperinsulinemia. Wound healing is delayed, and metabolic efficiency is increased. The strain carries the misty mutation (Dock7m) to aid in early identification of homozygotes.Read More +
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 4 to 8 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. Because Leprdb homozygotes are functionally sterile, the coat color marker misty (Dock7m) has been incorporated into stocks for maintenance of the diabetes mutation. The coupling double heterozygote, (Dock7m Leprdb/+ +, this strain) allows identification of homozygotes before the phenotype becomes severe.
The recessive misty mutation causes a mild dilution of coat color. On certain backgrounds, a white tail tip often accompanied by a belly spot is also present. Melanocytes from homozygous misty mice (Dock7m/Dock7m) have a highly dendritic shape, show deficient proliferation in culture and have much more melanin content. Fewer melanoblasts are found in primary cultures from Dock7m/Dock7m mice than from wildtype controls. Between two and five weeks of age, Dock7m/Dock7m mice are smaller than controls. At 35 days of age they are shorter, weigh 15% less on average, and have less inguinal adipose mass than controls. Misty homozygotes completely lack brown fat. Although platelet count, seratonin content and ATP content are normal, bleed time is increased and platelet AD levels are reduced in Dock7m/Dock7m homozygotes. (Woolley, 1941 and 1945; Truett et al. 1998; Sviderskaya et al. 1998.)
The strain was cryopreserved in 1990 at generation N6F36.
|Allele Synonym(s)||misty; Dock7m|
|Gene Symbol and Name||Dock7, dedicator of cytokinesis 7|
|Gene Synonym(s)||Gm430; ZIR2; RIKEN cDNA 3110056M06 gene; gene model 430, (NCBI); m; 3110056M06Rik; m; misty; 3110056M06Rik; mKIAA1771; LOC242555; EIEE23|
|Strain of Origin||DBA/J|
|Molecular Note||Crosses between mice homozygous for misty and for moonlight, which mapped to overlapping critical regions on Chr 4, demonstrated failure of the two mutations to complement one another. Once moonlight had been identified as a mutation of Dock7 (Dock7mnlt), sequence analysis of this gene from misty mice revealed a retrotransposon LTR insertion following nucleotide 2045 (numbering from the A of the transcription initiation codon) that interrupts exon 18 and shifts the reading frame after codon 682 so that ten incorrect amino acids are incorporated into the protein before its premature termination.|
|Allele Synonym(s)||Leprdb; diabetes|
|Gene Symbol and Name||Lepr, leptin receptor|
|Gene Synonym(s)||diabetes; OB-R; OB-RGRP; obese-like; obl; OBR; CD295; LEP-R; Leprb; LEPRD; LEPROT; obl; Modb1; leptin receptor gene-related protein; obese-like; db; Fa; Obr|
|Strain of Origin||C57BLKS/J|
|General Note|| |
Phenotypic Similarity to Human Syndrome: Gestational Diabetes J:219658
|Molecular Note||A G-to-T transversion in this allele created a donor splice site that causes abnormal splicing and a 106 nt insertion 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 using the B6-diabetes mouse strain in a publication, please cite the originating article(s) and include JAX stock #000699 in your Materials and Methods section.
|Homozygous, Heterozygous or Wild-type for Dock7<m> Lepr<db>|
We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.
Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.
|Frozen Mouse Embryo||$2,595.00 per straw or vial|
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