Hoodia Gordonii is known to contain a very special chemical compound, a steroidal glycoside, which enables the plant to act as an anorectic, an agent that suppresses appetite. It does this by inducing the sense of satiety in the brain, the sensation of fullness which leads the brain to switch off the desire for food. Having established that the Hoodia plant has this effect, and identifying the intriguing steroidal glycoside as the active ingredient in the plant, researchers then sought to establish exactly why and how the effect was caused.

Scientists studying Hoodia at Brown University in Rhode Island noticed that the steroidal glycoside it contains is similar in structure to a class of plant-derived compounds called cardiac glycosides. These substances are used to increase the force of contraction of the heart muscle and help maintain normal heart rate and rhythm, but they have a common side effect of loss of appetite, leading the researchers to feel that the actions of the Hoodia steroidal glycoside and the cardiac glycosides might be connected.

Cardiac glycosides act by stimulating a receptor molecule in the cells of the body called Na/K-ATPase, the function of which is to regulate the flow of sodium and potassium into and out of the cell using energy provided by a chemical called Adenosine Triphosphate (ATP). This process enables cells to perform muscle contraction, including heart muscle contraction, which is why cardiac glycosides are used for heart problems. But despite its similarities to these cardiac glycosides, studies on Hoodia's steroid glycoside failed to show any effect on the Na/K-ATPase receptor, indicating that the Hoodia's active ingredient appears not to act as a cardiac glycoside. The Hoodia compound also failed to show any effect on a wide range of other types of receptors, so at this time how it actually worked in the body was still a mystery.

The Brown researchers then tried a different approach and injected the steroidal glycoside directly into the brains of rats. The chosen location in the brain was the hypothalamus, the part of the brain controlling the body's basic functions, including appetite. The purpose of this was to determine whether the steroidal glycoside's appetite-suppressing effect was the result of direct action on the hypothalamus, and the answer to the question appeared to be yes. In multiple trials with the injected rats, food intake was reduced by 50–60% during the first 24 hours after the injections, and the effect, which was dose-dependent, lasted for about 24–48 hours.

The Brown researchers also discovered that the steroidal glycoside appeared to have more than doubled the level of the chemical Adenosine Triphosphate (ATP) in the hypothalamus. To test this further they put some rats on a restricted diet for 4 days, which decreased the ATP in the hypothalmus by 40%. This was understandable, because ATP is created in the body by the metabolism of food, so less food should result in less ATP. But when these underfed rats had the steroidal glycoside injected into their brains the ATP in the hypothalamus immediately rose to about normal.

The researchers had therefore shown that the steroidal glycoside does increase ATP levels in the hypothalamus. From this it seems reasonable to suggest that the mode of Hoodia's action in suppressing appetite appears to have been uncovered, that its active ingredient increases hypothalamic ATP and that this increased hypothalamic ATP is the key to inducing the sense of satiety in the brain.

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