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LETTER TO THE EDITOR |
Division of Nephrology
Department of Medicine
University of Florida
1600 Archer Road
Gainesville, FL 32610
E-mail: segalms{at}medicine.ufl.edu
Dear Sir:
We agree with Hine that more studies of the metabolic effects of fructose are needed, including its potential role in the polyol pathway, which is linked with diabetic complications, and as a potential agent that increases the risk of pancreatic and other cancers (1, 2). We also agree that fructose transporters, such as Glut 5, are widely expressed and are also upregulated by fructose, consistent with data that recurrent fructose exposure may lead to the increased release of uric acid (3) and to greater effects on triacylglycerols, body fat, and insulin resistance (4).
White, in contrast, makes the common error of trying to exonerate high-fructose corn syrup (HFCS) by comparing it with sugar, thus ignoring our key point that the problem rests with fructose rather than with HFCS per se. The fact is that total fructose intake has increased 30% over the past several decades because of the combined intake of both HFCS and sucrose, both of which contain approximately 50% fructose. The reason that studies compare fructose with glucose is to show that it is the fructose component that is associated with the development of the metabolic syndrome (5). Starch-based diets do not cause the metabolic syndrome, whereas the consumption of either fructose or sucrose rapidly cause features of the metabolic syndrome in humans and in animals. White should rest assured that we are not attacking the HFCS industry anymore than the sugar industry; our point is that it is the fructose content of foods that may have an important role in the epidemic of obesity and the metabolic syndrome (6).
White also tries to dismiss the huge amount of animal data indicating that fructose diets can induce the metabolic syndrome by stating that the doses used are physiologically irrelevant. Currently, the mean intake of fructose in our population is 
12% of total energy, which rises to 15% or more in children (7). Low doses of fructose (15%) also cause insulin resistance in rats if administered for 15 mo, whereas this is not observed with starch (8). The reason that higher doses are typically used is so that we can induce the metabolic syndrome rapidly (within weeks). Similarly, humans do not develop obesity within weeks of consuming a 15%-fructose diet; however, if 1000 kcal fructose is administered, insulin resistance can be induced within 1 wk (9). This concept of administering high doses to observe an effect in a short time period is commonly used in the biological sciences; indeed, the development of an accelerated model for slow virus disease had a key role in allowing Prusiner (10) to dissect the role of prions in disease, for which he received the Nobel prize.
Interestingly, however, there are several additional reasons why high doses of fructose are administered to rats. First, rats may be more resistant to the effects of fructose because fructose-induced hyperuricemia is blunted because of the presence of uricase (11). Indeed, hyperinsulinemia develops within 6 wk when 20%-fructose diets is administered to rats in which uricase is inhibited (12). Rats also make vitamin C, which blocks fructose-induced insulin resistance (13). We found that vitamin C also blocks the reaction of uric acid with various oxidants and neutralizes the effect of fructose or uric acid to induce oxidative stress in adipocytes (14). Finally, as noted by White, fructose is usually administered with glucose either as HFCS or as table sugar. Studies in animals have shown that glucose accelerates fructose absorption, as does the reverse (15), and indeed features of the metabolic syndrome can be induced in rats by feeding sucrose or fructose + glucose mixtures at levels of fructose less than that observed with fructose alone (W Mu, RJ Johnson, unpublished observations, 2008). Thus, we encourage future studies to examine the direct effects of sugar or HFCS on the induction of the metabolic syndrome as opposed to fructose alone because of the likelihood that greater toxicity will be observed for an equivalent dose of fructose.
ACKNOWLEDGMENTS
MSS and RJJ have a patent application pending for blocking fructokinase as a means of preventing obesity and for categorizing foods according to fructose index.
REFERENCES
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