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Department of Physiology University of Turku Kiinamyllynkatu 10 20520 Turku Finland E-mail: tommi.vasankari{at}vierumaki.fi
Dear Sir:
Elliott et al (1) wrote an interesting article concerning fructose, weight gain, and the insulin resistance syndrome. In that review they concluded that an increased consumption of fructose might be one of the environmental factors contributing to the development of obesity and the accompanying abnormalities of the insulin resistance syndrome. It is true that the prevalence of obesity in the United States and worldwide is increasing, and it is important to identify the acquired causes contributing to this increase. However, several lifestyle factors other than an increased consumption of fructose are much more probable contributors to the development of obesity (eg, a high intake of fat and minimal physical activity).
Elliott et al described a few mechanisms by which the consumption of dietary fructose might influence glucose metabolism and insulin resistance. However, they did not address the prolonged effects of dietary fructose on glucose metabolism, which are worthy of review. Type 2 diabetes (or, adult-onset diabetes) is one of the biggest health problems in the Western world, and it is suggested to be a consequence of increased energy intake and decreased physical activity. In persons with type 2 diabetes, the need for insulin is greater than that able to be produced by the pancreas. Therefore, the foods that produce a lower secretion of insulin (ie, foods that have a low glycemic index) are known to be beneficial for glucose metabolism. Koivisto and Yki-Jarvinen (2) studied the effects of dietary fructose (20% of calories as carbohydrate calories; 45–65 g/d for 4 wk) on insulin concentration and glycated hemoglobin in 10 patients with type 2 diabetes. In that study, subjects were fed—in a double-blind, randomized crossover design—a crystalline fructose or isocaloric complex carbohydrate (control) diet evenly as 4 meals or snacks per day while hospitalized. The mean diurnal blood glucose concentration decreased during both diets, but serum insulin concentration remained unchanged. Glycated hemoglobin, measured to determine glucose balance long term, improved only during the fructose diet (9.0% compared with 8.0%; P < 0.02) (2). In that study, insulin sensitivity also increased, by 34% (P < 0.05), during the fructose diet but remained unchanged during the control diet.
Even more long-term effects of a fructose diet on glycemic control were studied by Osei et al (3). They performed an outpatient study in 18 patients with type 2 diabetes who consumed either 60 g crystalline fructose/d (n = 9) or their usual meals (n = 9; control group) for 12 wk. Osei et al reported that both serum glucose and glycated hemoglobin concentrations progressively decreased in the group treated with fructose but had a tendency to increase in the control group during the study. The authors concluded that a slight improvement in glycemic control and alterations in the apoprotein composition that favor a decreased risk of coronary artery disease may occur with an increased consumption of fructose (3). The conclusion by Elliott et al that dietary fructose has only detrimental metabolic and endocrine effects is somewhat misleading. However, Elliott et al do suggest that much more research is needed to fully understand the metabolic effects of dietary fructose, particularly in humans.
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