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Dietary Factors and Hereditary Myocardial
Diseases
P. Di Nardo, M. Minieri, F. Carotenuto, R. Fiaccavento,
M. Zingarelli, C. Fantini, A. Bertoli, A. Fusco.
Dept Internal Medicine, Università di Roma
"Tor Vergata", Roma, Italy
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The action mechanism of nutritional factors are usually studied
in healthy animals and no information are presently available on the effect
of nutritional factors in cardiovascular hereditary diseases. In fact,
the presence of specific mutations has always been considered as exhaustive
explanation of the pathogenesis of hereditary diseases and the role of
other factors, such as diet, of marginal interest. Nevertheless, the different
human cardiomyopathic phenotypes of individuals sharing the same mutation
indicate that other genetic and/or environmental factors can play a fundamental
role in the pathophysiology of the disease. In the present study, we evaluated
the effects of different diets in hamsters (CMPH) affected by a hereditary
myocardial disease. Similarly to human beings, the disease determines the
progressive destruction of the myocardium leading animals to death when
aged 7-8 months. The administration of fresh vegetables and sunflower or
linen seeds from weaning prevents the animal death and the hamster lifespan
is prolonged until two years (i.e. the same that healthy animals). The
histopathologic evaluation of the myocardium showed that cardiomyopathic
tissue modifications are only minimally represented. In addition, several
molecular and biochemical parameters, typically characterizing the myopathic
phenotype, are reconverted to normality or substantially improved. In particular,
the presence in the diet of fresh vegetables modulate the expression of
genes coding for hormones (ANF), receptors (SERCA2), and structural (sarcoglycans,
dystroglycans, actin) and contractile proteins (myosin heavy chain, myomesin).
The improved quality of the myocardial tissue, restores a normal heart
contractile function and hemodynamics and the hamster lifespan lasts approximately
two years. Obviously, the diet does not eliminate the mutation that causes
the disease, but surely interferes with basic pathophysiologic mechanisms
of the disease.
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