Potential role of glycerol leading to rat fructose hypertension

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 mmHg 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); trigiyceridemia 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 ED50 to 12,13-phorbol dibutyrate in the fructose-glycerol group than in the control (P<0.001), glycerol (P<0.002), find 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).