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(Circulation. 2002;106:2486.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
From the Department of Hospital Laboratories, UMass Memorial Medical Center (C.R.K., L.M.S.), and Department of Pathology, University of Massachusetts Medical School (J.B.M., J.F.T), Worcester, Mass.
Correspondence to Charles R. Kiefer, PhD, Department of Hospital Laboratories, UMass Memorial Medical Center, One Biotech Park, Suite 200, 365 Plantation St, Worcester, MA 01605-2376. E-mail kieferc{at}ummhc.org
Background The Dahl sodium-sensitive hypertensive rat exhibits atherogenic lesions after the initiation of a high-sodium/high-fat diet. This study was designed to gauge the effect of a preadolescent high-fat diet on the postadolescent rate of atherogenesis after supplementation of the diet with sodium.
Methods and Results Fifty-three Dahl S male rats were assigned to 2 dietary groups for the postweaning to early adolescence period (3 to 12 weeks): 29 to a standard diet (low-fat/low-sodium) and 24 to a high-fat/low-sodium diet. At age 9 weeks (just after puberty), animals from the high-fat group exhibited a relatively diminished density of coronary elastic fibers. There was no evidence of either lipid or monocytic infiltration of the subendothelial space. At age 12 weeks, most or all of the remaining animals in both groups were switched to a high-sodium/high-fat diet and were sampled through the following 8 weeks for the appearance of arterial lipid. After the switch, the high-fatconditioned animals developed more extensive atherosclerotic pathological lesions more rapidly than their prepubertal standard-diet counterparts. The importance of the animals stage of maturation in this effect was underscored by the observation that delaying onset of the high-fat diet to early adolescence resulted in no ultimate difference from the pubertal controls in elastic fiber density.
Conclusions The maturation-dependent high-fat conditioning of these postweanling rats correlated with an accelerated rate of atherogenesis on the initiation of the high-sodium/high-fat diet, possibly as a direct result of an alteration in arterial elasticity.
Key Words: coronary disease elasticity hypercholesterolemia hypertension
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