Hg. Preuss et al., SUGAR-INDUCED BLOOD-PRESSURE ELEVATIONS OVER THE LIFE-SPAN OF 3 SUBSTRAINS OF WISTAR RATS, Journal of the American College of Nutrition, 17(1), 1998, pp. 36-47
Objective: Since the majority of studies concerned with sugar-induced
blood pressure elevation have principally been short-term, the present
investigation followed the effects of heavy sucrose ingestion on syst
olic blood pressure (SEP) and related parameters over the lifespan of
three substrains of Wistar rats.Methods: Two hundred twenty-five rats(
75 spontaneously hypertensive rats (SHR), 75 Wistar Kyoto rats (WKY),
75 Munich Wistar rats (WAM)) were given one of five diets. The baselin
e diet in terms of calories derived 32% from sucrose. 33% from protein
, and 35% from fat. The remaining four diets derived their calories as
follows: a high sugar-lbw protein diet-52% of calories from sucrose,
15% from protein, and 33% from fat; a high sugar-low fat diet-53% of c
alories from sucrase, 37% from protein, and 10% from fat; a low sugar-
high protein diet-11% calories from sucrose, 56% from protein, and 33%
from fat, and a low sugar-high fat-13% of calories from sucrose, 32%
from protein, and 55% from fat. Results: All substrains showed the hig
hest systolic blood pressure when ingesting the two diets highest in s
ucrose, The highest sugar-induced SEP elevation, which remained over t
he lifespan of all substrains, was found in SHR. WKY had an intermedia
te elevation. WAM showed the lowest responses, although the average el
evation of 6-8; mm Hg was statistically significant. The following par
ameters could nor be correlated with long-term elevation of SEP: body
weight, catecholamine excretion, renal function, and plasma renin acti
vity. Only insulin concentrations correlated: insulin concentrations w
ere consistently higher To the two groups of WKY and WAM consuming the
high sucrose diets, Conclusions: High dietary sucrose can chronically
increase SEP in three substrains of Wistar rats. Increased concentrat
ions of circulating insulin were found in WKY and WAM suggesting that
the glucose/insulin system was involved. at least in these two substra
ins, in the maintenance of high SEP levels during chronic, heavy sugar
ingestion.