ob/ob mouse

Two white mice both with similar sized ears, black eyes, and pink noses. The body of the mouse on the left, however, is about three times the width of the normal sized mouse on the right.
A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right)

The ob/ob or obese mouse is a mutant mouse that eats excessively and becomes profoundly obese. It is an animal model of type II diabetes. Identification of the gene mutated in ob led to the discovery of the hormone leptin, which is important in the control of appetite.

The first ob/ob mouse arose by chance in a colony at the Jackson Laboratory in 1949.[1] The mutation is recessive. Mutant mice are phenotypically indistinguishable from their unaffected littermates at birth, but gain weight rapidly throughout their lives, reaching a weight three times that of unaffected mice. ob/ob mice develop high blood sugar, despite an enlargement of the pancreatic islets and increased levels of insulin.[2]

The gene affected by the ob mutation was identified by positional cloning.[3] The gene produces a hormone, called leptin, that is produced predominantly in adipose tissue. One role of leptin is to regulate appetite by signalling to the brain that the animal has had enough to eat.[4] Since the ob/ob mouse cannot produce leptin, its food intake is uncontrolled by this mechanism.

See also

References

  1. ↑ Ingalls AM, Dickie MM, Snell GD (December 1950). "Obese, a new mutation in the house mouse". J. Hered. 41 (12): 317–8. PMID 14824537.
  2. ↑ Lindström P (2007). "The physiology of obese-hyperglycemic mice [ob/ob mice]". ScientificWorldJournal 7: 666–85. doi:10.1100/tsw.2007.117. PMID 17619751.
  3. ↑ Zhang Y, Proenca R, Maffei M, Barone M, Leopold L, Friedman JM (December 1994). "Positional cloning of the mouse obese gene and its human homologue". Nature 372 (6505): 425–32. doi:10.1038/372425a0. PMID 7984236.
  4. ↑ Friedman JM, Halaas JL (October 1998). "Leptin and the regulation of body weight in mammals". Nature 395 (6704): 763–70. doi:10.1038/27376. PMID 9796811.

External links

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