Morphofunctional and immunological cardiac evaluation of protein restriction on rat offspring

Cardiovascular diseases affect a large part of the population during adulthood. Several epidemiological and experimental studies have demonstrated an association between maternal protein restriction and a marked risk of developing heart disease during early intrauterine and postnatal life. Maternal nutritional conditions act by modulating the microenvironment, thus favoring adaptive processes of the fetal organism for development to occur. However, the physiological profile is established in this period and its effects can be observed in the long term. In the present study, the cardiac muscles of 15-day-old offspring of Wistar rats subjected to maternal protein restriction during pregnancy and/or lactation were evaluated to identify possible cardiac changes relevant for heart disease in adulthood. The offspring of restricted female rats during pregnancy had a lower birth weight. Male offspring subjected to restriction during pregnancy and lactation showed an increase in the concentration of H2O2, a reduction in the expression of the Mn-SOD enzyme, and a greater expression of beta-MHC and Connexin 43. There was also an increase in the MPO enzyme activity in the tissue. It was observed that the effects of protein restriction are sex-specific, since the cardiac muscle of male animals showed alterations suggestive of oxidative stress, hypertrophy, signs of tissue inflammation, and increased expression of important proteins in intercellular communication. These changes characterize the ongoing cardiac remodeling process. Finally, the data revealed that the lactation phase accentuated harmful effects on the cardiac tissue of the offspring. (c) 2022 Elsevier GmbH. All rights reserved.

Automated summary

Cardiovascular diseases affect a large part of the population during adulthood. This study demonstrates an association between maternal protein restriction and the risk of developing heart disease in offspring. The effects of protein restriction on the cardiac muscles are sex-specific, with male offspring showing oxidative stress, hypertrophy, and signs of tissue inflammation.