ob/ob Mice (JAX® Mice Strain) Details
Also known as B6 ob, these animals are homozygous for the obese spontaneous mutation, Lepob (often referred to as ob or ob/ob), show obesity, hyperphagia, transient hyperglycemia, glucose intolerance, and elevated plasma insulin. Ob/ob mice are also hypometabolic, hypothermic, and often subfertile. Hormone production from both pituitary and adrenal glands is increased, and wound healing is impaired. Ob/ob mice are commonly used to model phases 1 and 2 of diabetes type II, as well as obesity. The obesity is characterized by a growth in the number and size of adipocytes. Although hyperphagia furthers the obesity, homozygotes gain weight and deposit surplus fat even when restricted to a diet sufficient for normal weight maintenance in lean mice.
Growth chart data should be used as a guideline only.
The shaded areas on each chart are the mean weight plus or minus one standard deviation at a given age averaged across all production facilities. This represents approximately 67% of the population, with the remaining 33% falling outside of this weight range.
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At approximately 4 weeks old, mice which are homozygous for the obese spontaneous mutation (Lepob; or ob/ob) are first identifiable.
Homozygous ob/ob mice gain weight quickly, and may approach a weight of 3 times that of control mice. Besides obesity, these mouse models exhibit hyperphagia, a condition of hyperglycemia, similar to diabetes.
They display glucose intolerance, increased levels of plasma insulin, weakened wound healing, subfertility, and an increase in hormone production (both in adrenal and pituitary and glands). Moreover, these ob/ob mice become hypothermic and hypometabolic.
Obesity in these animals can be seen through an increase in both adipocyte number and size. Adipose tissue transplants in Lepob homozygotes guard against obesity, normalize insulin sensitivity, and restore fertility.
Homozygotes have an unusually low tolerance for stimulation of pancreatic islet insulin secretion. Female homozygotes exhibit reduced uterine and ovarian weights, diminished ovarian hormone production and hypercytolipidemia in follicular granulosa and endometrial epithelial tissue layers (Garris et al., 2004).
Though hyperphagia contributes to obesity in ob/ob mice, homozygotes gain excess weight and deposit excess fat even when limited to a diet sufficient for normal weight preservation in lean mice. Hyperinsulinemia does not progress until after the rise in body weight, and is likely a result from it. Similar to the diabetic mutation (Leprdb), manifestation of the diabetic syndrome is clearly reliant on on genetic background.
Hyperglycemia is only transient, (decreasing about 14 to 16 weeks) on the C57BL/6J background. On the C57BLKS background, obese homozygotes become severely diabetic with regression of islets and early death.
Injection of recombinant leptin into obese homozygotes dramatically decreases weight and food consumption, while increasing the energy spending and energy and and reinstates fertility in male ob/ob mice.
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