It is widely accepted by the medical community that
obesity seriously increases risks for several life-threatening
diseases, though this idea has its detractors (see:
The Obesity Myth). It was thought that the excess
body fat that must be carried about by the obese person put such a strain on the
heart and other organs which eventually led to this increased
risk. More recently, however, scientists have been looking at the
adipose tissue (aka
FAT) as not just extra weight to be carried around, but as an
organ secreting
chemical messengers.
One of the most well-known of these chemical messengers is leptin. As is bound to happen when researchers discover ways to turn formerly svelte laboratory mice into the rodent equivalent of Jabba the Hutt and vice versa, the media jumped upon leptin as a potential silver bullet to our obesity problems. It was not, as we nearly always find out, that simple, however ongoing research into leptin is a promising route to understanding obesity in humans.
Leptin is a protein consisting of 167 amino acids in the human variety. The amount of circulating leptin is directly proportional to the amount of fat in the body, making it a crucial component in long term body weight regulation. Leptin receptors are found in the hypothalamus and the protein has several effects. It counteracts the effects of the two potent feeding stimulants neuropeptide Y and anandamide (the latter of which binds to the same receptors as THC and thus appears to be the feeding stimulant responsible for the munchies). It also promotes the creation of α-MSH, an appetite suppressant. In addition to its regulating effects on appetite, leptin appears to be a regulator of reproductive function by stimulating the secretion of gonadotropin-releasing hormone, which could be the mechanism that causes women with very low body fat to cease menstruation. Mutations in the gene for leptin are rarely found in obese people, but obese people usually have higher levels of leptin than would be expected, indicating that they are in some way insensitive to leptin.
The existence of leptin and its long-term effects on the appetite is fairly discouraging to dieters--just another reminder that you cannot fool your body. Your fat cells are constantly sending information to your brain about your level of body fat, causing your appetite to adjust accordingly. As would be expected, dieting decreases levels of leptin and--even more good news!--the higher the initial leptin level, the more it declined with dieting. This may help explain why most dieters eventually regain the weight previously lost and why crash and fad dieting is counterproductive to weight control.
Sources:
http://arbl.cvmbs.colostate.edu/hbooks/pathphys/endocrine/bodyweight/leptin.html
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/L/Leptin.html
http://www.rockefeller.edu/pubinfo/leptinlevel.nr.html