Mouse Obesity Model with Modified Leptin Receptor

Description: The hormone leptin regulates food intake, metabolic rate and endocrine function. Disruption of leptin or its receptor molecule abolishes normal regulatory mechanisms, leading to obesity and endocrine dysfunction. The leptin receptor activates certain signal transduction pathways that mediate its normal roles in the cell. The inventors have discovered that certain signaling pathways of the leptin receptor play a role in control of body weight, while distinct pathways control other functions such as fertility. To distinguish these pathways, transgenic mice were created in which the long form of the leptin receptor is mutated to replace the tyrosine at position 1138 with a serine. Phosphorylation of Tyr 1138 is known to mediate activation of the transcription factor STAT3, which triggers the weight control pathways. Mice mutated at this locus become obese without losing other functions such as fertility. Clinical & Commercial Utility: The available technology features transgenic mice, homozygous for the serine 1138 substitution in the long form leptin receptor. Like db/db mice, the leprS1138 homozygotes are hyperphagic and obese, but unlike db/db mice, are fertile, long in size, and less hyperglycemic. These mice therefore comprise a model of human obesity that may have distinct advantages over other commonly available models.
The creation of the leprS1138 homozygote mice are described in Bates, et al., Nature (2003) 421:856-859. Joslin is the owner of a pending U.S. patent application, which covers these mice and methods of treating obesity by modulating leptin receptor-STAT3 signaling.

Type of Offer: Licensing

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