These mice carry a spontaneous mutation at the Lep locus on a C57BLKS/J background and are characterized by obesity, hyperphagia, hyperglycemia, glucose intolerance, and elevated plasma insulin. On the C57BLKS background homozygotes become severely diabetic with regression of islets and early death.Read More +
Mice homozygous for the obese spontaneous mutation (Lepob, commonly referred to as ob or ob/ob) are first recognizable at about 4 weeks old. Homozygous mutant mice increase in weight rapidly and may reach three times the normal weight of wildtype controls. In addition to obesity, mutant mice exhibit hyperphagia; a diabetes-like syndrome of hyperglycemia, glucose intolerance, and elevated plasma insulin; subfertility; and increased hormone production from both pituitary and adrenal. They are also hypometabolic and hypothermic. The obesity is characterized by both an increased number and size of adipocytes. Although hyperphagia contributes to the obesity, homozygotes gain excess weight and deposit excess fat even when restricted to a diet sufficient for normal weight maintenance in lean mice. Hyperinsulinemia does not develop until after the increase body weight and is probably the result of it. Homozygotes do have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young preobese animals. As is the case with the diabetes mutant (Lepdb), manifestation of the diabetic syndrome is strikingly dependent on genetic background. On the C57BLKS background Lepob/Lepobhomozygotes become severely diabetic with regression of islets and early death. Cloning of the Lep gene has made possible the production of recombinant leptin. Injection of this protein into Lepob/Lepob homozygotes sharply reduced body weight, decreased food intake, and increased energy expenditure.
|Allele Type||Spontaneous (Null/Knockout)|
|Allele Synonym(s)||ob; ob/ob|
|Gene Symbol and Name||Lep, leptin|
|Strain of Origin||STOCK Mlphln a Tgfawa1 Cdh23v Ednrbs|
|Molecular Note||Sequencing of RT-PCR products revealed a nonsense mutation in arginine codon 105 (p.R105*) resulting from a C-to-T point mutation. The 16 kDa leptin protein, expressed predominantly in adipose tissue of normal mice, is missing from homozygous mutant mice (J:29081).|
When using the BKS-obese mouse strain in a publication, please cite the originating article(s) and include JAX stock #000696 in your Materials and Methods section.