LONG-TERM FRUCTOSE CONSUMPTION ACCELERATES GLYCATION AND SEVERAL AGE-RELATED VARIABLES IN MALE RATS

Fructose intake has increased steadily during the past two decades. Fr uctose, like other reducing sugars, can react with proteins through th e Maillard reaction (glycation), which may account for several complic ations 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 acc ess to water or 250 g/L solutions of fructose, glucose or sucrose. Ear ly glycation products were evaluated by blood glycated hemoglobin and fructosamine concentrations. Lipid peroxidation was estimated by urine thiobarbituric reactive substances. Skin collagen crosslinking was ev aluated by solubilization in natural salt or diluted acetic acid solut ions, and by the ratio between beta- and alpha-collagen chains. Advanc ed glycation end products were evaluated by collagen-linked fluorescen ce in bones. The ratio between type-III and type-I collagens served as an aging variable and was measured in denatured skin collagen. The te sted sugars had no effect on plasma glucose concentrations. Blood fruc tose, cholesterol, fructosamine and glycated hemoglobin levels, and ur ine lipid peroxidation products were significantly higher in fructose- fed rats compared with the other sugar-fed and control rats. Acid-solu ble collagen and the type-III to type-I ratio were significantly lower , whereas insoluble collagen, the beta to alpha ratio and collagen-bou nd fluorescence at 335/385 nm (excitation/emission) were significantly higher in fructose-fed rats than in the other groups. The data sugges t 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.