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Studies using laboratory rodents have consistently shown that dietary fructose supplementation causes diabetes (reviewed in Rizkalla, 2010). For example, rats with free access to 10% fructose water developed glucose intolerance, hypertriglyceridemia, hyperinsulinemia, and ?-cell apoptosis (Maiztegui, Borelli, Raschia, Zotto, and Gagliardino, 2009). In agreement with these results, feeding six healthy, non-obese, young males a high-fructose diet for one week caused a significant reduction in plasma nonesterified fatty acid (NEFA) and increased triacylglyceride levels (Abdel-Sayed, Binnert, Le, Bortolotti, Schneiter, and Tappy, 2008). This finding suggests a fructose-rich diet suppresses lipid oxidation and thereby contributes to ectopic fat deposition in organs such as the liver. When 20 healthy subjects were fed a diet supplemented with either glucose or fructose, only the glucose diet resulted in weight gain (Silbernagel, Machann, Unmuth, Schick, Norbert, Haring, et al., 2011). However, the high fructose diet significantly increased fasting glucose levels, insulin insensitivity (also glucose), and serum triglyceride levels, which are all metabolic changes consistent with increased diabetes risk.
Evidence against Fructose Causing Type 2 Diabetes
A prospective cohort study of 15,792 men and women, with either Caucasian or African-American ethnicities and between the ages of 45 and 64, revealed no significant association between sweetened beverage consumption and diabetes onset during a nine-year follow-up period (Paynter, Yeh, Voutilainen, Schmidt, Heiss, Folsom, et al., 2006). Even the authors were surprised by this finding, in light of the results from studies. The authors suggested that age might be a factor, but the epidemiological studies presented here included