Accumulation of advanced glycation endproducts in aging male Fischer 344 rats during long-term feeding of various dietary carbohydrates.

The observation of accelerated collagen glycation in association with enhanced progression of many age-associated diseases in hyperglycemic subjects has led researchers to propose a role of glycation in the aging process. Although short-term studies in healthy animals suggest that feeding a diet high in fructose may increase serum glucose concentrations and increase glycemic stress, the effects of a long-term feeding, i.e., life span, are unknown. This study was designed to evaluate the long-term effects of dietary carbohydrates on serum and tissue markers of glycemic stress. Three-month-old male Fischer 344 rats were given free access to or restricted to 60% caloric intake of one of five isocaloric diets that contained as their carbohydrate source either cornstarch, glucose, sucrose, fructose or equimolar amounts of fructose and glucose. Rats were killed at 9-, 18- or 26-mo of age. Glycated hemoglobin, serum glucose and fructosamine levels were measured as markers of serum glycemic stress. Collagen-associated fluorescence and pentosidine concentrations were measured in skin, aortic, tracheal and tail tendon collagen as markers of advanced glycation endproducts (AGE). The source of dietary carbohydrate had little effect on markers of glycemic stress and the accumulation of AGE. Restricting the amount of calories consumed resulted in lower serum glucose concentrations, glycated hemoglobin levels and pentosidine concentrations in tail tendon collagen. Our data suggest that the rate of collagen glycation is tissue-specific. These results suggest that long-term feeding of specific dietary carbohydrates does not alter serum glucose concentrations or the rate of collagen glycation. Rather, age-related accumulation of AGE is more closely related to caloric intake.