M. Kemi et al., The relative protective effects of moderate dietary restriction versus dietary modification on spontaneous cardiomyopathy in male Sprague-Dawley rats, TOX PATHOL, 28(2), 2000, pp. 285-296
The relative protective effects of modifying dietary protein, fat, fiber, a
nd energy content vs moderate food or dietary restriction (DR) on spontaneo
us cardiomyopathy of Charles River male Sprague-Daw ley (SD) rats was evalu
ated at 1 and 2 years. For 2 years, SD rats a ere fed Purina Rodent Chow 50
02 (21.4% protein. 5.7% fat, 4.1% fiber, 3.1 kcal/g) or a modified rodent c
how 5002-9 (13.6% protein. 4.6% fat. 15.7% crude fiber, 2.4 kcal/g) ad libi
tum (AL) or by moderate DR at approximately 65% of the caloric intake of th
e AL group fed the 5002 diet. Serum lipids, carcass composition, and organ
weights were evaluated and hearts were qualitatively and quantitatively exa
mined microscopically for male SD rats at 1 and 2 years. Cardiomyopathy was
characterized by the colocalization of myocardial degeneration, the develo
pment of subepicardial, perivascular. subendocardial. acid interstitial fib
rosis, and mononuclear inflammatory cell infiltration that increased by inc
idence and severity in an age-dependent manner from 1 to 2 years. SD rats f
ed the 5002 diet AL had the greatest heart weights and the most severe card
iomyopathy, with the highest myocardial fibrotic index. These parameters we
re relatively decreased in the AL 5002-9 diet, the DR 5002 diet, and the DR
5002-9 diet rats at 1 and 2 years. Regardless of the type of diet fed, bot
h AL groups had the most severe cardiomyopathy by 2 years. Moderate DR allo
wed isocaloric comparisons of the relative effects of modified diets on sur
vival, obesity, and heart disease. Only slight improvements in the severity
and progression of spontaneous cardiomyopathy were seen by modification of
the protein, fiber; fat, and energy content of the diet if fed AL. However
, moderate DR with either diet was more effective than changing the diet co
mposition in preventing and controlling the progression of cardiomyopathy i
n male SD rats.