While the control of food intake occurs in the brain, the portions of the brain related to appetite control respond to nerve signals sent from the liver.Specifically, this relates to the content of adenosine triphosphate or ATP content of the liver. ATP is the most elemental form of energy, and all energy-producing foods, such as carbs, fats, and even protein, are eventually converted into ATP. When the liver is replete in its ATP content, the message is sent to the brain, and no hunger signals are sent out from the brain's appetite center.This pathway was initially discovered in rats, who were provided with a form of fructose known to deplete ATP stores in the liver. When that happened, the rats got ravenously hungry.When you eat a meal, the ATP content of the liver rises, and the faster it rises, the less hungry you'll be, and you will also eat less in subsequent meals.
The major food element needed by the liver to synthesize ATP is the mineral phosphorus. In fact, ATP is nothing more than an adenosine molecule with three attachments of phosphorus.When the bonds that attach phosphorus to adenosine are broken, energy is released.But when meals are consumed, particularly meals containing a higher simple carb content, insulin is released.Insulin promotes the uptake of phosphorus into other tissues besides the liver, where it's used in reactions that involve attaching phosphorus to activate various compounds.When this happens,less phosphorus is available to help synthesize liver ATP. What would happen if one meal contained a significantly higher phosphorus level--would this higher level be enough to promote increased liver ATP content, which would in turn, turn down appetite signals for later meals?
One reason why fructose is linked to excess bodyfat is that it sequesters phosphorus,making it unavailable for use in liver ATP synthesis. This, in turn, promotes greater hunger and a tendency to overeat. In a recent study, adding "preloads" or extra phosphorus to a meal resulted in a 27% reduction in energy intake at the next meal. The technique worked even better when sugars, such as sucrose and fructose were consumed.Adding phosphorus to such sugar meals resulted in a 35% reduction in energy intake at the next meal. How phosphorus does this isn't clear, but it probably relates to increased liver ATP synthesis. Lower levels of ATP are common in those who are obese, and this low level drives overeating, while promoting the less usage of energy in exercise, thus perpetuating obesity. This effect of phosphorus in helping to curtail appetite may explain why some studies show that eating dairy products, which are rich in both calcium and phosphorus, may help promote fat losses.High protein foods are also usually rich in phosphorus content. This explains why the common warning about how eating too much protein leads to calcium losses is bogus. That effect only occurs when pure protein foods are eaten. The phosphorus naturally contained in most high protein foods not only prevents the loss of calcium, but also helps retain it in the body, explaining why recent studies show that eating more protein helps maintain bone mass. Eating a higher protein meal leads to greater satiety or appitite reduction. The key factor for this effect of protein might be the phosphorus content of protein foods, which aids in the rapid synthesis of liver ATP, which results in easier control of appetite
Obeid OA, et al.Increased phosphorus content of preload suppresses ad libitum energy intake at subsequent meal.Int J Obesity2010: in press.
