ob/ob mice
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Mice that are homozygous for the mutant ob gene; their body fat produces no leptin, and they become very obese; discovered in 50s
> eat more than control mice; they convert calories to fat more efficiently, and they use their calories more efficiently
> Coleman hypothesized that they lack a critical hormone that normally inhibits fat production and maintenance
> in 1994, Friedman characterized and cloned the gene that is mutated in ob/ob mice
> found this gene expressed only in fat cells, and they characterized the protein it normally encodes, a peptide hormone they named leptin
>SO because of the mutation, the mice lacked leptin
> led to exciting hypothesis that perhaps leptin is a negative feedback signal normally released from fat stores to decrease appetite and increase fat metabolism
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Motor neurons
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homeostasis
What will be an ideal response?