Yu and Lee (1987) [Yu and Lee, 1987: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1025947&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/3321712)] cited research showing that the sequestration of inorganic phosphate (Pi) that occurs, in the liver (or kidneys, assuming that it's a parenteral fructose load or is administered more directly to the kidneys), in response to a fructose load decreases serum phosphate by causing an increase in the cellular uptake of phosphate. Researchers have also found that the administration of exogenous phosphate can prevent or reduce the depletion of liver ATP that results from the administration of fructose [Morris et al., 1978: (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=372529&blobtype=pdf)(http://www.ncbi.nlm.nih.gov/pubmed/618911)] or a fructose analog [Rawson and Friedman, 1994: (http://www.ncbi.nlm.nih.gov/pubmed/8024030)]. Morris et al. (1978) cite some interesting research, on the first two pages, and say that fructose rapidly depletes serum phosphate/phosphorus and that the ATP depletion that can be induced in the kidneys, in response to fructose administration, can produce a state that resembles Fanconi's syndrome. So it sounds like fructose has the potential to also increase the urinary excretion of phosphate, by reducing phosphate reabsorption by the proximal tubule epithelial cells (Fanconi's syndrome is characterized by renal phosphate wasting/loss of phosphate in the urine). Rawson and Friedman (1994) found that exogenous phosphate prevented the depletion of ATP that occurs in response to the administration of a phosphate-sequestering fructose analog, and the authors also cited research showing that liver ATP depletion reliably stimulates "feeding behavior" in rodents. I've seen that mentioned in a lot of other articles, and it's relevant to the research on phosphate depletion and the metabolic syndrome (insulin resistance, etc.). I haven't looked at the full text of this article yet, but Zhou et al. (1991) [Zhou et al., 1991: (http://www.ncbi.nlm.nih.gov/pubmed/1848327)] found that phosphate depletion, in pancreatic islets (presumably they were looking at the intracellular changes in the beta cells in the islets), increased the cytosolic calcium concentration and decreased the ATP levels and the ATP/ADP ratio and the magnitude of the glucose-induced secretion of insulin secretion. There's a good amount of research on that effect of phosphate, as evidenced by the similar articles listed alongside that abstract. There's an article showing decreases in phosphofructokinase activity in beta cells that are phosphate-depleted [Perna et al., 1991: (http://www.ncbi.nlm.nih.gov/pubmed/1837585)], and those authors found evidence of phosphate-sensitive changes in the Km of the enzyme for fructose-1-phosphate. Yu and Lee (1987) cited research that apparently had shown that hyperventilation can decrease serum phosphate by increasing the intracellular pH and thereby activating phosphofructokinase. They're saying that activating phosphofructokinase increases the overall activities of glycolytic enzymes other than phosphofructokinase and that that activation serves to sequester Pi in phosphorylated, glycolytic intermediates (thereby disinhibiting the cellular uptake of Pi from the blood). I remember reading that phosphofructokinase is pH-sensitive, but it sounds like Pi regulates it directly, also, and I remember reading that Pi produces allosteric activation of one or more glycolytic enzymes.
I think that a lot of people could probably prevent phosphate depletion by just drinking slightly more milk, limiting fructose consumption (it's difficult to do, but processed foods generally contain more fructose than unprocessed foods, although fruit contains a lot of fructose). I hate to say it, but fruits and orange juice contain a lot of fructose, and it's not necessarily good for a person to eat fruits. But a lot of processed foods probably contain more fructose and more fat, etc. I'm just saying that everyone seems to think fruits and vegetables are the same, but vegetables don't generally have fructose in them. The carrot is the only vegetable I know of that has a high glycemic index (it has a lot of simple sugars in it), but I personally wouldn't eat carrots because of their high content of preformed vitamin A. That's, incidentally, a downside of drinking tons of milk, too, in my view, but I don't think it's likely to be a problem for most people. But there are case reports of intracranial hypertension (elevated intracranial pressure and psychiatric symptoms) occurring in people who ate only carrots and didn't even take vitamin A supplements. I wouldn't take any supplemental vitamin A or beta-carotene, because of the risk of some sort of occult, low-level effect on the choroid plexuses, but that's just me.
There's an interesting article I found that discusses the use of "organic phosphates," including fructose 1,6-bisphosphate and other phosphorylated sugars, to treat hypophosphatemia, and the authors said that organic phosphates tend to not become as extensively bound to calcium, in the GI tract, as Pi from sodium phosphate, for example, does. The same concept would apply to ATP disodium, in my opinion, because some of it is likely to be absorbed intact. There's also research showing that fructose diphosphates (1,6- and 2,6- etc.) can serve as energy substrates [Marchesani et al., 2000: (http://www.ncbi.nlm.nih.gov/pubmed/10773790)], and I used to think that that research sounded bogus. But the phosphorylated forms can exert almost the opposite effect of fructose, to some extent, because many or most of the adverse effects of fructose result from its effect of depleting intracellular Pi. There are some articles showing neuroprotective effects of fructose diphosphates, in vitro, at least. It's really interesting because one's first thought (my first thought, at least) is that there couldn't possibly be any advantage to the use of fructose diphosphate, in comparison to glucose, as an energy substrate. I didn't think phosphorylated sugars could be transported into cells intact, but maybe they don't have to be. It could just be that the provision of the extra phosphate is the only thing that's necessary, to prevent the intracellular phosphate depletion (and concomitant decreases in serum or extracellular-fluid phosphate) that would otherwise occur in response to the administration of fructose alone.
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