Fetal programming occurs during the gestational age when exposure to environmental stimuli can cause long-term changes in the fetus, predisposing it to develop chronic
non-communicable diseases (CNCD) in adulthood. Herein, we summarized the role of low-calorie or high-fat diets during pregnancy as fetal programming agents that induce
intrauterine growth restriction (IUGR), amplified de novo lipogenesis, and increased
amino acid transport to the placenta, which favor the CNCD onset in the offspring. We also outlined how
maternal obesity and
gestational diabetes act as fetal programming stimuli by reducing
iron absorption and
oxygen transport to the fetus, stimulating inflammatory pathways that boost
neurological disorders and CNCD in the progeny. Moreover, we reviewed the mechanisms through which
fetal hypoxia elevates the offspring's risk of developing
hypertension and
chronic kidney disease in adult life by unbalancing the renin-angiotensin system and promoting kidney cell apoptosis. Finally, we examined how inadequate
vitamin B12 and
folic acid consumption during pregnancy programs the fetus to greater adiposity,
insulin resistance, and
glucose intolerance in adulthood. A better understanding of the fetal programming mechanisms may help us reduce the onset of
insulin resistance,
glucose intolerance,
dyslipidemia,
obesity,
hypertension,
diabetes mellitus, and other CNCD in the offspring during adulthood.