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Journal of the American College of Nutrition, Vol. 17, No. 1, 36-37 (1998)
Published by the American College of Nutrition


Original Paper

Sugar-Induced Blood Pressure Elevations Over the Lifespan of Three Substrains of Wistar Rats

Harry G. Preuss, MD, Mohmed Zein, MD, Philip MacArthy, MD, Donald Dipette, MD, Sharda Sabnis, MD and Joseph Knapka, PhD

Nephrology Division (H.G.P., M.Z., P.M.), Georgetown University Medical Center, Washington, DC
Department of Medicine, Georgetown University Medical Center, Washington, DC
University of Texas Medical Branch (D.P.), Galveston, Texas
Nephropathology Section (S.S.), Brookville, Maryland
Walter Reed Army Institute of Pathology, Washington DC; and (J.K.), Brookville, Maryland

Address reprint requests to: Harry G. Preuss MD, FACN, Georgetown University Medical Center, Bldg D, Rm 371, 4000 Reservoir Road, NW, Washington, DC 20007

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 systolic blood pressure (SBP) 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 baseline 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-low protein diet—52% of calories from sucrose, 15% from protein, and 33% from fat; a high sugar-low fat diet—53% of calories from sucrose, 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 highest systolic blood pressure when ingesting the two diets highest in sucrose. The highest sugar-induced SBP elevation, which remained over the lifespan of all substrains, was found in SHR. WKY had an intermediate elevation. WAM showed the lowest responses, although the average elevation of 6–8 mm Hg was statistically significant. The following parameters could not be correlated with long-term elevation of SBP: body weight, catecholamine excretion, renal function, and plasma renin activity. Only insulin concentrations correlated: insulin concentrations were consistently higher in the two groups of WKY and WAM consuming the high sucrose diets.

Conclusions: High dietary sucrose can chronically increase SBP in three substrains of Wistar rats. Increased concentrations of circulating insulin were found in WKY and WAM suggesting that the glucose/insulin system was involved, at least in these two substrains, in the maintenance of high SBP levels during chronic, heavy sugar ingestion.

Key words: Hypertension: sugar-induced, insulin perturbations, hypertension




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