<h3>Background</h3> The development of the heart is a sensitive and dependent process of stem cells present during its maturation. Changes in the population of these cells through modifications in the intrauterine environment due to a metabolic program, such as during pregnancy of obese women is something of concern. It is estimated that 30% of pregnant women are obese and that 40% of women gain excessive weight during pregnancy. Thus, the objective of this work is to analyze the impacts of maternal obesity on the heart of the offspring in neonate Swiss mice. <h3>Methods</h3> After birth, litters were adjusted to nine pups and divided into overfeeding Group - nine pups until the 3rd day, when the litter was reduced to three female pups, and control Group with nine pups. Three months old females of both groups were mated to healthy males and their offspring were euthanized at the day of birth, resulting in the Offspring Control Group (OCG) and Offspring Overfed Group (OOG). Biometric parameters were analyzed, and fragments of the heart were used to analyze fibrosis by Picro-Sirius Red stanning and to analyze the population of c-kit and sca-1 cells. The results were expressed as mean ± SEM, analyzed by t-student test. <h3>Results</h3> OOG showed, at birth, 25% increased body mass compared to OCG. However, there was no difference in naso-anal length between groups, reflecting an increase of 93% in the Lee Index of OOG compared to OCG. Although the cardiac mass was 35% decreased in OOG, the analysis of collagen deposition in the heart showed an increased interstitial fibrosis (196%) in this group compared to the OCG. In addition, the quantification of cardiac stem cells demonstrated an increase of 229% in the c-kit+ cells and an increase of 218% in the sca-1+ cells when compared to the OCG. <h3>Conclusion</h3> Together, results demonstrate that maternal metabolic programming negatively impacts offspring at birth, altering cardiac development, making the heart more immature at birth, as well as increasing adverse remodeling, which may be related to the development of cardiovascular diseases in adulthood.