|M.Sc Student||Shilovitzky Orit|
|Subject||Long-Term Fructose Consumption: Presence of Advanced|
Glycation Endproducts, Oxidative Stress and Renal
|Department||Department of Biotechnology and Food Engineering||Supervisors||Professor Emeritus Shmuel Yannai (Deceased)|
|Mr. Moshe Werman|
The increasing use of fructose in the food industry raises concern, because of its reactivity with amino groups through the Maillard reaction (glycation), which leads to the formation of advanced glycation endproducts (AGEs). AGEs modify protein structure and stimulate negative cellular responses. They accumulate slowly with age and markedly in diabetes and renal failure.
Normally, AGEs are cleared by the kidney. We evaluated the effect of long-term (17 months) fructose drinking on AGEs accumulation, oxidative stress and renal function, compared to water consumption, in male ICR mice.
Fructose consumption increased drinking and urine volumes, daily caloric consumption and reduced food consumption in a concentration-dependent manner. Fructose intake elevated body weight and decreased relative kidney weight. Fructose has no influence on urine and plasma fructoseamine levels, while it causes a significant increase in urinary and plasma fructose content. Continuous fructose intake resulted in accumulation of AGEs in kidney (Bowman’s capsule, glomerular and tubular basement membrane, mesangium, tubular epithelial cells, and between the collecting tubules) and in plasma. Urinary pentosidine levels decrease as fructose intake increases and as age progresses. Fructose consumption had no effect on urinary albumin, but increased plasma albumin and kidney protein concentrations. Fructose intake was followed by elevated clearance rate of creatinine and urea, increased kidney, urine and plasma carbonyl stress, and lowered kidney antioxidant enzymes activity.
Our study suggests that long-term fructose consumption causes an increase in protein susceptibility to glycation, induces AGEs accumulation in the kidney and hampers normal renal function.