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This diagram is from Neuroscience: Exploring the Brain by Bear, Connors, and Paradiso.

Although the results of the 1940s study were interesting, they were not exactly physiologically relevant in terms of feeding behavior. Then, in the 1960s Douglas Coleman conducted a classic experiment in which he used genetically obese mice (ob/ob). He hypothesized that the ob gene encoded a protein hormone that signaled satiety. Because ob/ob mice lacked both copies of this gene, and therefore the resulting protein product, these mice remained insatiable. They overate to increase their perceived "low" fat reserves. Coleman used a technique known as parabiosis to anatomically and physiologically fuse an ob/ob mouse and a normal mouse so that they shared a blood supply, and thus, any hormones in the blood. Interestingly, the extra fat storage on the ob/ob mouse was greatly reduced, which demonstrated that some sort of hormone most likely played a role in regulating the motivation to overeat.




Publication Information


Coleman, D.L.


Effects of Parabiosis of Obese with Diabetes and Normal Mice

Diabetologia 9: 294-298


Next: the leptin controversy.

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Return to the project home page Neural Reward, Energy Homeostasis, and Addiction-like Compulsive Eating

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