The hypothalamus is the neural center for the regulation of food intake. One area of the hypothalamus consisting of the lateral nuclei, controls hunger, or the craving for food. Another area consisting of the ventromedial nuclei, controls satiety, or the feeling of fulfillment. Therefore, drugs or supplements that act on the hypothalamus can act as an anorectic (appetite reducing) agent. Prescription drugs like amphetamine and fenfluramine function by increasing the level of brain catecholamines and 5-hydroxytrypt­amine (serotonin), which causes a feeling of fullness and suppresses the appetite, respectively Some dietary supplements could alter the levels of neurotransmitters in the hypothalamic region and regulate food intake.

The body may also produce its own satiety chemical or hormone that suppresses the appetite. The Set-Point Theory suggests that fat cells prefer to maintain a certain size. When there is a reduction in the size of the adipocyte due to dieting, a signal is sent to the hypothalamus resulting in an increase in appetite. As the fat cell regains its size, another signal is sent to the hypothalamus, which instructs the hypothalamus to reduce or stop the desire to eat.

The maintenance of a perfect body weight is a survival mechanism for higher organisms including mammals. Furthermore, the maintenance of body weight requires both the maintenance of energy and nutrient balance. This means that the diet must contain both adequate amounts of calories, macronutrients (carbohydrate, protein, and fat), and micro nutrients (vitamins and minerals).

Research using rodents may have discovered the signal for the Set-Point Theory. The signal is called leptin, and it appears to have a dual role, it decreases food intake and increases energy expenditure resulting in an increase in fat oxidation. When rats are bred to be deficient in this hormone, it causes them to overeat and become obese. When this hormone is administered to rats, it causes them to stop eating and increases fat oxidation, resulting in fat loss but not a loss in lean tissue (i.e., muscle). However, human research indicates that the hormone is not the problem, but rather the transporter. Obese individuals appear to develop a resistance to leptin that is similar to insulin resistance. Therefore, it may be impractical to expect leptin administration to humans to be a viable means of controlling obesity. If the transporters are already saturated or downregulated from excessive endogenous leptin, it does not make sense to provide more. Therefore, research has begun to focus on the leptin transporter and binding site in hopes of discovering the post-binding signaling cascade and any potential defects in this system. Leptin research is interesting and may one day provide a drug to control obesity, but this probably won’t happen for many years. For more information on leptin, read the excellent reviews by Hwang et al. and by requier and Tappy. Although several mechanisms could be used as a target for fat loss, most of the dietary supplements targeted as a fat loss agent do not have scientific research to support their claims.


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