It shuts off the neurotransmitters in response to leptin, a hormone released by fat cells.
In this case, however, the calorie-restricted animals did not stop producing leptin in their adipose tissue.
Somehow, therefore, a fully functioning leptin system can still produce a dangerous urge to overeat.
But the explanation lies in the rapid adjustment of the leptin system to the environment.
Leptin has several roles, but one is to encourage cells to oxidise lipids and thus destroy them.
Expecting an unrestricted food supply to persist, it downgrades its leptin levels in order to maximise fat consumption and storage.
At the end of their binges, all the rats were injected with leptin, in order to test the adipose tissue's response.
The rats who dined carte blanche, on the other hand, did reduce the amount of leptin that their adipose tissue produced.
In support of this hypothesis, the researchers point to studies on mice whose leptin receptors have been broken by genetic mutations.
For example, in the cases of the heart-muscle cells and pancreatic cells mentioned above, dosing them with leptin keeps them healthy.
Leptin has led to a revolution in the study of why some of us are fat and others of us are thin.
When injected with the protein leptin, which the obese gene codes for, they shed up to one-third of their weight in fat.
The story of leptin is told on the BBC Science programme Horizon.
The problem is that obese humans very rarely show a mutation in either the gene for leptin or that for its receptor.
Dr Rossetti wondered if external factors, such as the availability of food in the environment, might affect the amount of leptin produced.
Leptin production, meanwhile, grows along with the mass of the adipose tissue.
The biggest embarrassment: the fat-fighting hormone Leptin, widely hyped as a cure for obesity in the mid-1990s but abandoned in trials by Amgen in 2000.
These results thus shed light on why, in a series of clinical trials conducted last autumn, leptin treatment did not prove uniformly effective (let alone miraculous).
Dr Rossetti had previously established that this tends to reduce an animal's leptin production, presumably because the appropriate sensors detect that there is already enough of it around.
In a healthy mouse (one with working leptin receptors) even a diet that is 60% fat does not cause a build-up of lipids anywhere except in the adipose tissue.
The market for an anti-fat pill would be enormous, and the quest for one will continue even though Dr Rossetti's research shows that the leptin-regulation system is more complex than had been realised.
In what is, admittedly, the least-tested part of their thesis, Dr Unger and Dr Scherer argue that other cells react to this increase in leptin concentration by becoming resistant to the hormone's effects.
Dr Unger and Dr Scherer suggest that this failure of the leptin mechanism, particularly its role in oxidising lipids, is crucial to the development of metabolic syndrome, and that it is a pathology of adipose tissue that has become overloaded.
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