LebanonFood intake is believed to be partially controlled by hepatic signals related to adenosine triphosphate (ATP) status. We hypothesized that increased phosphorus content of one meal can stimulate hepatic ATP synthesis of the next meal, which in turn contributes to satiation. This hypothesis was tested by measuring the energy intake after phosphorus addition to several preloads. The phosphorus content of the different preloads was found to be inversely related to the energy intake at a subsequent meal, although the exact mechanism behind such effects was not studied. Such findings point to a potential role for phosphorus in the control of food intake. In humans, food intake is known to be controlled by both physiological and non-physiological factors, in which the former are believed to be partially governed by signals originating from the liver. 1,2 There is accumulating evidence of a negative relationship between hepatic ATP level and eating behavior; the changes in hepatic ATP (energy status) is thought to be transduced into neural or hepatic vagal afferent activity, which is transmitted to the central nervous system and which eventually controls food intake. 1,2 This relationship is based on data from several studies, in which the administration of a fructose analog, 2,5-anhydro-D-mannitol (2,5-AM), which causes a decline in the amount of inorganic phosphate necessary for ATP synthesis in the liver 3 ; or L-ethionine (which traps adenine and thus lowers ATP production) 4 to rats was found to stimulate eating behavior. Moreover, the hepatic ratio of ATP to ADP (adenosine diphosphate) (or the phosphorylation potential of the cell) was reported to be a more sensitive index of cellular energy status than ATP content. 5 This relationship implies that an increase in postprandial hepatic ATP synthesis triggers satiation, and the faster that the hepatic ATP increases, the greater the reduction in energy intake. In the postprandial state, phosphorus is utilized for the phosphorylation of many metabolites and its uptake by extrahepatic tissue is stimulated by insulin release, and thus its availability for hepatic ATP production may be compromised. Therefore, it is reasonable to postulate that the provision of a surplus amount of phosphorus in one meal would improve the hepatic phosphorus status or would offset any reduction caused by the second meal. This in turn would accelerate hepatic ATP synthesis, leading to an early termination of the eating episode.Increased consumption of fructose, mainly in the form of high-fructose corn syrup, has paralleled the rise in obesity and this has raised a concern over fructose's involvement in weight gain. 6 Fructose is known to have 'phosphatesequestering' capacity, by virtue of which the phosphate attaches covalently to organic molecules, rendering it unavailable to participate in other essential metabolic reactions, including the regeneration of ATP. 7,8 This was demonstrated in humans, in whom the intravenous administration of fructose (250 mg per kg of body weight over 5 ...