Relationship between renal and cardiovascular changes in a murine model of glucose intolerance

Nutrition is an important variable which may affect the risk for renal disease. We previously showed that a high fructose diet in mice produced hypertension and sympathetic activation [8]. The purpose of this study was to determine if a fructose diet altered renal function. A high fructose diet for 12 weeks impaired glucose tolerance, but caused no change in body weight, blood glucose or plasma insulin. Impairment in renal function was documented by the almost two fold increase in urinary protein excretion (Control: 6.6 ± 0.6 vs. Fructose: 15.0 ± 0.7 mmol protein/mmol creatinine; p < 0.05) which was also accompanied by increases in urinary volume. The diet produced little change in renal histology, kidney weight or kidney weight/body weight ratio. Urinary excretion of angiotensin II/creatinine (Control: 78.9 ± 16.6 vs. Fructose: 80.5 ± 14.2 pg/mmol) and renal angiotensin converting enzyme activity (Control: 9.2 ± 1.6 vs. Fructose: 7.6 ± 1.0 ACE units) were not different between groups. There was a positive correlation between mean arterial pressure (r = 0.7, p = 0.01), blood pressure variability (BPV) (r = 0.7, p = 0.02), low frequency BPV component (r = 0.677, p = 0.03) and urinary protein excretion. Results show that consumption of a high fructose diet in mice had deleterious effects on renal function, which were correlated with cardiovascular changes.