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 alpha and betaII (with respect to the
glycerol group).