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One objection to the idea of a regulatory system with a set point was that a stable weight 
can be achieved in other ways (Bolles, 1990; Garrow & Stalley, 1975; Harris, 1990; Wirtshafter 
& Davis, 1977). Any negative feedback loop will do, they argued. Bolles (1990) made this point 
vividly: When a cat gets too fat, it can no longer catch rats, so it loses weight. That a fat cat is 
slow is not due to a regulatory system. Weight constancy might be due to one or more negative 
feedback loops that exist for other reasons. 
Is weight constancy accidental? Set point regulation of body fat by the brain requires that 
the brain “know” the amount of body fat, just as set point regulation of room temperature (by a 
thermostat) requires that the thermostat “know” the room temperature. The set point idea 
implies, in other words, that something reaching the brain must vary with the amount of body fat. 
The Bolles et al. view – that weight constancy is an accident – does not require such a signal. For 
this reason, the discovery of leptin, a hormone whose blood concentration varies with amount of 
body fat (Woods, Schwartz, Baskin & Seeley, 2000), strongly favored the set-point view. Leptin 
has just the properties needed for regulation. 
When body fat is below set point, research suggests that two changes take place. First, 
hunger increases. Humans report more hunger than usual (Keys et al., 1950); rats eat more often 
(Levitsky & Collier, 1968). Second, allesthesia decreases. Food stays pleasant longer. In humans, 
this is revealed by pleasantness ratings and meal length (Cabanac, Duclaux & Spector, 1971; 
Cabanac & Frankham, 2002); in rats, by meal length (Levitsky & Collier, 1968). Both changes 
tend to increase body fat.

 
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http://evan.stasis.org/odds/whatmakesfoodfattening.pdf

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