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Strain

B6.BKS(D)-Lepr^db/J

Summary

Data Summary

Official Name	B6.BKS(D)-Lepr^db/J
Common Name	B6.BKS(D)-Lepr^db/J
Description	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.
Creation Method	spontaneous
Background	C57BL/6J
Breeding Type	intercross
Phenotype Description	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. Homozygous mutant mice are polyphagic, polydipsic, and polyuric. The course of the disease is markedly influenced by genetic background. A number of features are observed on the C57BLKS background, including an uncontrolled rise in blood sugar, severe depletion of the insulin-producing beta-cells of the pancreatic islets, and death by 10 months of age. Exogenous insulin fails to control blood glucose levels and gluconeogenic enzyme activity increases. Peripheral neuropathy and myocardial disease are seen in C57BLKS Leprdb homozygotes. 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 difference s in obesity-induced diabetes susceptibility. The diabetes mutation is a result of a point mutation in the leptin receptor gene, Lepr. This point mutation promotes abnormal splicing, creating a stop codon that shortens the intracellular domain of the receptor, such that its signaling capacity is curtailed. The ligand, leptin, has been shown to be a key weight control hormone that is mutated in the mouse obesity mutation, Lepob. Morbid obesity with hypogonadism is seen in patients with mutations in the Leptin receptor gene, however the incidence is rare.

Type	Count
Genomics - Modifications	1
Experiments	5

Genomic Information

Gene	Allele 1	Allele 2	Protocol
Lepr	point mutation - transversion	point mutation - transversion	Not Specified

OrderID	Order	Investigator	Experiment	Status	Measurements
19683	19683	Pascal Sirvent	Hyperglycemic clamporder #19683 March 2016	Completed	5429
836	836	Aamir Zuberi	Hyperglycemic Insulinemic Clamp Order #836 1/31/05	Completed	1439
18536	18536	Jin Shengkan	Liver lipids in db/db mice treated with Methionine and Choline Deficient (MCD) Diet or MCD plus niclosamide for 3 weeks	Completed	32
19683	19683	Pascal Sirvent	Sable Energy Balance #19683 3/21/16	Completed	420
7748	7748	Henry Lopez	Systolic function in db/db C57BL6 mice	Completed	145

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