Evaluation of the effect of maternal consumption of a high-fat diet on cardiac function in adult offspring.
Hyperlipidic diet, Metabolic programming, Cardiac function, Angiotensin II.
The increase in weight in the world population has taken alarming proportions, because the rate of obesity, both in people and in domestic animals, is increasing. This scenario is worrying among mothers, as they can program their lineage for the long term, increasing the risk of chronic diseases, such as cardiovascular disease. Previously, it was demonstrated in our research group that mother rats that consumed a high-fat diet during pregnancy and lactation, generated offspring with increased body mass, adiposity, hyperleptinemia after weaning, in addition to impaired cardiac function at 30 days of age . Some physiological mechanisms seem to be involved in the development of cardiovascular alterations. Increased cardiac adrenergic activity, for example, can lead to heart failure. On the other hand, the renin angiotensin system (RAS) expressed in the heart seems to trigger mechanical stress and cardiac remodeling, through the overexpression of Angiotensin II (Ang II) and activation of its type 1 receptor (AT1). Therefore, the aim of this work is to evaluate whether maternal consumption of a high-fat diet promotes cardiac dysfunction, and to investigate the renin angiotensin system (RAS) expressed in the hearts of male and female offspring in adulthood. For this, Wistar rats consumed a control diet (9% lipids, group C) or a high-fat diet (29% lipids, group DH) for 8 weeks before mating, during pregnancy and lactation. Group C gave rise to offspring C, and group DH gave rise to offspring DH. From weaning to adulthood, all offspring consumed only the control diet. At 180 days of age, cardiac function was assessed by means of echocardiogram and isolated heart analysis using the Langendorff technique (with increasing concentrations of isoproterenol – 0.3 to 1000 nM). The animals were euthanized, body weight, white adipose reservoirs (epididymal, inguinal and retroperitoneum) and hearts were collected and weighed. Biochemical and molecular analyzes (RIA and qPCR) are being performed, using samples from the left ventricle (LV), and the expression of AT1 and AT2 receptors is being evaluated using the Western Blotting technique. Females and males of the DH offspring did not show changes in body mass, adiposity and heart weight. However, these animals had impaired cardiac function, and only males of the DH offspring had increased cardiac adrenergic responsiveness. Biochemical and molecular analyzes to investigate the expression of Ang II, and the protein expression of its AT1 and AT2 receptors, are still ongoing, as well as analyzes of the expression of Nppn, β-MHC and α-MHC mRNA. To date, our results suggest that maternal consumption of a high-fat diet promotes cardiac dysfunction in adult offspring, and increased heart adrenergic sensitivity only in male offspring.