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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Long-term fructose consumption accelerates glycation and several age-related variables in male rats.

Fructose intake has increased steadily during the past two decades. Fructose, like other reducing sugars, can react with proteins through the Maillard reaction (glycation), which may account for several complications of diabetes mellitus and accelerating aging. In this study, we evaluated the effect of fructose intake on some age-related variables. Rats were fed for 1 y a commercial nonpurified diet, and had free access to water or 250 g/L solutions of fructose, glucose or sucrose. Early glycation products were evaluated by blood glycated hemoglobin and fructosamine concentrations. Lipid peroxidation was estimated by urine thiobarbituric reactive substances. Skin collagen crosslinking was evaluated by solubilization in natural salt or diluted acetic acid solutions, and by the ratio between beta- and alpha-collagen chains. Advanced glycation end products were evaluated by collagen-linked fluorescence in bones. The ratio between type-III and type-I collagens served as an aging variable and was measured in denatured skin collagen. The tested sugars had no effect on plasma glucose concentrations. Blood fructose, cholesterol, fructosamine and glycated hemoglobin levels, and urine lipid peroxidation products were significantly higher in fructose-fed rats compared with the other sugar-fed and control rats. Acid-soluble collagen and the type-III to type-I ratio were significantly lower, whereas insoluble collagen, the beta to alpha ratio and collagen-bound fluorescence at 335/385 nm (excitation/emission) were significantly higher in fructose-fed rats than in the other groups. The data suggest that long-term fructose consumption induces adverse effects on aging; further studies are required to clarify the precise role of fructose in the aging process.[1]


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