Published online May 8, 2016. doi: 10.5409/wjcp.v5.i2.172
Peer-review started: September 6, 2015
First decision: October 8, 2015
Revised: January 25, 2016
Accepted: February 14, 2016
Article in press: February 16, 2016
Published online: May 8, 2016
Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, pre-eclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity.
Core tip: The adverse outcomes on the offspring born from altered gestation are already known. The consequences of these perturbations have been demonstrated even after many decades from birth. In this review we summarize gestational conditions associated to fetal programming and elucidate the mechanisms involved in such kind of occurrence. We also describe to what extent oxidative stress (OS) is involved in a very wide spectrum of genetic, metabolic, and cellular responses, through the gene expression regulation, and cell growth modulation. By virtue of these properties, OS has been nominated as the lowest common denominator of adult disease programming.