Mice homozygous for the obese spontaneous mutation, Lepob (commonly referred to as ob or ob/ob), exhibit obesity, hyperphagia, transient hyperglycemia, glucose intolerance, and elevated plasma insulin. They are also hypometabolic, hypothermic, and subfertile. Wound healing is impaired and hormone production from both pituitary and adrenal glands is increased. This strain is used to model phases I and II of diabetes type II and obesity. Obesity is characterized by an increase in the 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.Read More +
Mice homozygous for the obese spontaneous mutation, (Lepob; commonly referred to as ob or ob/ob), are first recognizable at about four weeks of age. Homozygous mutant mice gain weight rapidly and may reach three times the normal weight of wild-type controls. In addition to obesity, mutant mice exhibit hyperphagia, a diabetes-like syndrome of hyperglycemia, glucose intolerance, elevated plasma insulin, subfertility, impaired wound healing, and an increase in hormone production from both pituitary and adrenal glands. They are also hypometabolic and hypothermic. The obesity is characterized by an increase in both adipocyte number and size. Adipose tissue transplants in Lepob homozygotes protect them from obesity, normalize insulin sensitivity, and restore fertility. 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 in body weight, and probably results from it. Homozygotes have an abnormally low threshold for stimulation of pancreatic islet insulin secretion even in very young pre-obese animals. Female homozygotes exhibit decreased uterine and ovarian weights, decreased ovarian hormone production and hypercytolipidemia in follicular granulosa and endometrial epithelial tissue layers (Garris et al., 2004).
As is the case with mice carrying the diabetes mutation (Leprdb), manifestation of the diabetic syndrome is strikingly dependent on genetic background. Hyperglycemia is only transient, (subsiding around 14 to 16 weeks) on the C57BL/6J background. On the C57BLKS background, obese homozygotes (Stock No. 000696) become severely diabetic with regression of islets and early death. Injection of recombinant leptin into obese homozygotes sharply reduces body weight, decreases food intake, increases energy expenditure, and restores fertility in male mice.
Leptin can regulate bone mass through a central, neuroendocrine signaling pathway. Similar to the effects of aging in humans, homozygotes exhibit muscle hypoplasia (quadriceps), increased marrow adipogenesis and decreased bone mass in the hindlimbs (Hamrick et al., 2004).
The obese mutation, ob, arose spontaneously in strain V/Le at The Jackson Laboratory, Bar Harbor, Maine in 1949, and has been backcrossed to C57BL/6J for more than 45 generations.
|Allele Type||Spontaneous (Null/Knockout)|
|Allele Synonym(s)||ob; ob/ob|
|Gene Symbol and Name||Lep, leptin|
|Gene Synonym(s)||LEPD; OB; OBS; ob; obese; obese|
|Strain of Origin||STOCK Mlph |
|General Note|| |
Phenotypic Similarity to Human Syndrome: Metabolic Syndrome J:219470.
|Molecular Note||Sequencing of RT-PCR products revealed a nonsense mutation in codon 105 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 maintaining a live colony, these mice are bred as heterozygotes. Females homozygotes are infertile, and males exhibit a reduced ability to mate.
|Please inquire about possible genotypes.|
The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided,
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