Drugs, eating disorders and diets are methods used by overweight people to lose weight. In their desperation to shed pounds, they are willing to do anything. Treating obesity is an industry all by itself.

High protein diets for example, produce weight loss by restricting carbohydrates to induce metabolic stress. This harmful stress simulates the condition of starvation and causes the body to metabolize its long-term energy reserves (fat). This is not a healthy method to lose weight and also deprives the body of the healthy antioxidants embedded in the fibers of carbohydrates.

Over the past decade a large number of receptors and compounds in the brain have been targeted for the treatment of obesity.  With the obesity market approaching $4 billion this is not surprising.

The current pharmaceutical approaches to obesity have centered on centrally acting molecules that modify hunger, appetite or satiety.

The regulation of body weight is controlled by the appetite or satiety center, located in the hypothalamus. Most weight loss drugs work by acting on these nerve centers. Others, target the intestine and prevent the absorption and utilization of fat.


The best method to reduce weight is to lower caloric intake and increasing physical activity.  This process may take more time than the other methods but it is the only one that improves health.


In addition to burning more calories, exercise produces beta-endorphins and other small protein molecules, called neuropeptides (cholescystokin). These compounds interact with satiety center receptors in the hypothalamus to suppress appetite and inhibit further eating.

Research in neuronal pharmacology and receptor binding models provide novel new mechanisms for weight reduction drugs follow. neurotransmitter operate in specific areas of the brain and their ability to selectively either bind or act antagonistic to these receptors provide the basis for these drugs pharmacological MO’s.


Diet drugs can target the brain to suppress appetite or the digestive system to prevent dietary absorption or raise core temperature to increase metabolism. A few can even target adipose tissue to promote its loss. Drugs can increase metabolic rate, stimulate the breakdown of body fat or in the case of the prescription drug Xenical or its OTC version Alli, act as a lipase inhibitor. These two drugs inhibits the absorption of fat in the intestine and forces its removal from the body without obtaining any of its calories.


Meredia, Rimonabant, Redux, lipocortin, thermogenene, synthetic beta-adrenergic agonists, leptin, 5-HT, neuropeptide Y, melanocortin or  bombesin are all compounds and drugs that are involved with the brain’s neural chemistry regarding hunger and appetite.


Orlistat, Alli,  targets the digestive tract.


Orlistat is a potent inhibitor of lipase, an enzyme crucial to the digestion of long-chain triglycerides. Orlistat binds with the lipase receptor site rendering the enzyme inactive.

Lipase inhibition results in the removal of fat in the feces instead of being deposited as body fat.


There is a confluence of nerves that meet in an area of the brain known as the hypothalamus. This area is responsible for interpreting and coordinating nerve transmissions and detecting momentary changes in chemistry based.

Nerve transmissions depend on the nuerotransmitters serotonin, dopamine and norepinephrine.  The monitoring process depends on hormones, neuropeptides, minerals, amino acids and sugar, which are detected via a vast network of membrane receptors. These receptors provide the sites for the various ions, metabolites, hormones and proteins to bind to. This binding information is processed along with all the visual, auditory, olfactory, gustatory and proprioceptive signals that emanate from the five senses.


The hypothalamus is responsible for regulating appetite, mood, and pleasure. Drugs, foods, advertisements and thoughts can either stimulate appetite or repress it. They produce their effects through the phenomenon of receptor binding.

Specifically, a stimulus (image, sight, smell, taste, thought or chemical) signals a series of events that culminate in the binding of their respective receptors in the hypothalamus.

The neural chemistry of the hypothalamus is thus a prime target of pharmacetical companies that attempt to develop diet drugs to repress appetite.


Receptors are normally bound to a series of native ligands, it is through these bindings that appetite is regulated according to the body’s set point.  Set point is based on fat levels.

The main native compounds involved with monitoring the amount of fat in the body and adjusting appetite accordingly, are the proteins, leptin and orexin neuropeptide Y and gherlin. The concentration of these neuropeptides determines how much eating is necessary and whether there already is enough energy stored in the body.

Leptin is a small hormone produced inside adipose tissue. Fat cells release this protein when their cytoplasm is full of fat. The amount of leptin released is correlated to the amount of fat the cell contains. The more fat the cell contains, the higher the amount of leptin that is release where it circulates to the brain and is monitored by nerve cells involved with energy regulation.

Once bound, leptin represses the urge to eat since it indicates that there already is enough energy stored in the body. A high level of leptin reflects a full storage of fat in the body.

While leptin is produced inside of fat cells, its effect is on the central nervous system where it suppresses appetite and prevents further eating.

Leptin opposes the effects other neuropeptides. Leptin binds with receptors that normally bind to appetite stimulating ligands. Notable is the anandamide receptor, which the canabanoids of marijuana and neuropeptide Y bind to.  These two compounds are known to stimulate hunger and eating. When leptin occupies these sites, it blocks the drive to eat. Leptin analogues are under investigation as a possible therapy for obesity.


Ghrelin is another hormone produced outside the brain, in this case they are manufactured by the cells lining the stomach.  Gherlin counters the effect of leptin.

Once ghrelin reaches the brain, it stimulates appetite. Ghrelin levels are high just before meals, which promotes the desire to eat. Ghrelin levels decrease as the meal is consummed, signalling am end to eating. Due to its promotion of appetitie, ghrelin has become a hot target for pharmaceutical intervention.  Both the receptor to which it binds creating ghrelin antagonists.


Ghrelin levels drop following the consumption of fructose rich meals. This may explain the overeating seen in kids since the 1980’s, when fructose was first introduced as a replacement sweetner.


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