Hormonal Biomarkers for Evaluating the Impact of Fetal Growth Restriction on the Development of Chronic Adult Disease
Abstract The hypothesis of fetal origins to adult diseases proposes that metabolic chronic disorders, including cardiovascular diseases, diabetes, and hypertension originate in the developmental plasticity due to intrauterine insults. These processes involve an adaptative response by the fetus to changes in the environmental signals, which can promote the reset of hormones and of the metabolism to establish a “thrifty phenotype”. Metabolic alterations during intrauterine growth restriction can modify the fetal programming. The present nonsystematic review intended to summarize historical and current references that indicated that developmental origins of health and disease (DOHaD) occur as a consequence of altered maternal and fetal metabolic pathways. The purpose is to highlight the potential implications of growth factors and adipokines in “developmental programming”, which could interfere in the development by controlling fetal growth patterns. These changes affect the structure and the functional capacity of various organs, including the brain, the kidneys, and the pancreas. These investigations may improve the approach to optimizing antenatal as well as perinatal care aimed to protect newborns against long-termchronic diseases.