This article, describing the findings of a panel discussion in which people compared some of the effects of fructose and sucrose, is noteworthy:
http://www.webmd.com/food-recipes/news/20081211/high-fructose-corn-syrups-bad-rap-unfair
If one reads the article carefully, one can see that the panel is saying that fructose is no more likely to contribute to obesity than fructose. There is, first, the statement that sucrose, a sugar that is the predominant disaccharide in table sugar, is about 50 percent fructose by mass. Assuming no part of a dose of sucrose is absorbed as a disaccharide (and it looks like it isn't), then it's probably valid to assume that eating 100 grams of sucrose will produce plasma fructose and glucose levels that are the same as those that would be produced by eating 50 grams of free fructose and 50 grams of free glucose. I'm not sure that this would always be the case, given that the pharmacokinetics of sugars can differ among individuals, but let's suppose that it would be. Then there's the statement that high-fructose corn syrup is about 55 percent fructose, meaning that sucrose is no more likely than high-fructose corn syrup to produce obesity.
I don't, personally, agree with this statement, and, in my opinion, the issue is the amounts of fructose that people are more or less forced to eat (not the comparison to sucrose), given the large amounts of fructose that are in so many foods. High-fructose corn syrup is added to so many products that it's almost impossible, in my view, to avoid eating significant amounts of fructose. But the implication of the article is that fructose is metabolized in the same way as glucose, derived from "free" glucose or glucose from complex carbohydrates, is.
Fructose has been shown to produce metabolic changes that can be very different from the changes that glucose, given to the same individual animal or person, produces, and these differences can be particularly significant in animals or people who have ingested glucose in a slow-release form, such as some cereal grains might provide, as opposed to a quickly-released form. The article above mentions an article showing that fructose is more efficiently converted into triglycerides. This is likely to be the case, in my opinion, and there are hundreds if not thousands of research articles that have shown that to be the case. Fructose can also cause significant depletions of both adenine and guanine nucleotides from the liver and, when it's infused directly into the kidneys, from the kidneys as well. These effects of fructose have been known for many years.
I don't have time to post the references/links to all the research, but the study of metabolism doesn't, in my view, boil down to the adding up of calories in and calories out. The depletion from the liver of ATP, in particular, and purine nucleotides in general can be very significant in response to fructose infusion or ingestion. The mechanisms underlying two major fructose-induced metabolic effects--namely ATP depletion and increase in fatty acid synthesis--are fairly well-understood. Here's one article that discusses the mechanisms to some extent. The idea is that fructose enters the liver (or, in this case, the kidneys) en masse, sequesters phosphate (inorganic phosphate, Pi) by its conversion into monophosphorylated and diphosphorylated metabolites (mostly fructose-1-phosphate, in this article, but also glycerol-1-phosphate, as monophosphorylated metabolites), and, as a result of phosphate depletion, reduces the amount of phosphate that's available for maintaining ATP. ATP depletion per se leads to the loss of purine nucleotides, and then the nucleotides are converted into uric acid. There might be other mechanisms, and I'll try to read up on the topic. The uric acid that the nucleotides are converted into is, incidentally, very unlikely to be responsible for the metabolic syndrome, in many cases (I've discussed this in previous postings). I don't have time to go into the explanations, but here are the articles discussing the phosphate depletion mechanism as a mechanism by which fructose ingestion can lead to the depletion of ATP, GTP, and purines overall:
http://www.jbc.org/cgi/content/abstract/255/17/8239
Pubmed Unique ID: (http://www.ncbi.nlm.nih.gov/pubmed/6773936?dopt=Abstract)
This article, below, is actually really interesting and discusses the sequestration of phosphate, as fructose-1-phosphate, in response to fructose loading, or as glycerol-1-phosphate, in response to glycerol, as a mechanism that leads to adenine nucleotide depletion from the liver. That might be relevant for understanding the adverse effects, namely ATP depletion or a reduction in the ATP/(total adenine nucleotide) ratio (or in the so-called adenylate charge), that could potentially result from the excessive accumulation of exogenous purines in the liver (or from exogenous ribose, although ribose hasn't been shown to cause nearly the same degree of adenine nucleotide depletion that xylitol and fructose and glycerol produce). There would be more purines to buffer the phosphate-sequestration-induced losses, but the effect might occur. Here's that article, though, discussing phosphate sequestration, by fructose and other metabolic intermediates, as a mechanism for purine nucleotide depletion:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1896274
(pubmed unique id: http://www.ncbi.nlm.nih.gov/pubmed/17324122)
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