Potential Role of Glycerol Leading to Rat Fructose Hypertension

Abstract

Abstract —A fructose-enriched diet promotes hypertension in rats. We thought that an enhancement of the glycolytic and/or lipid disorder (s) that raise blood pressure could be the cause. Therefore, we studied 4 groups of Sprague-Dawley rats (±200 g): (1) control rats received a standard diet and tap water; (2) the glycerol group of rats received a standard diet and 0.54 mol/L glycerol in tap water; (3) the fructose group was given a fructose-enhanced diet (chow had 55% fructose instead of dextrin) and tap water; and (4) the fructose-glycerol group was given the fructose-enhanced diet and 0.54 mol/L glycerol in drinking water. At the end of the second week, the findings were as follows. Blood pressure was 149±2 mm Hg in the fructose-glycerol group versus 129±2 ( P <0.001), 131±2 ( P <0.001), and 140±3 ( P <0.005) mm Hg in the control, glycerol, and fructose groups, respectively. Insulinemia was higher in the fructose-glycerol group than the control ( P <0.001), glycerol ( P <0.001), and fructose groups ( P <0.001); triglyceridemia was higher in the fructose-glycerol ( P <0.02), fructose ( P <0.05), and glycerol groups ( P <0.02) than the control group. Thoracic aorta rings showed a lower ED 50 to 12,13-phorbol dibutyrate in the fructose-glycerol group than in the control ( P <0.001), glycerol ( P <0.002), and fructose groups ( P <0.001). In conclusion, glycerol-fructose administration resulted in hypertriglyceridemia, hyperinsulinemia, and increased vascular sensitivity to 12,13-phorbol dibutyrate (with respect to the control group), and significantly greater expression of protein kinase C α and βII (with respect to the glycerol group).