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. Author manuscript; available in PMC: 2016 Mar 26.
Published in final edited form as: Cell. 2015 Mar 26;161(1):93–105. doi: 10.1016/j.cell.2015.02.021

Figures 2/3. Mechanisms linking fetal nutrient supply to later phenotypes.

Figures 2/3

Uteroplacental insufficiency decreases availability of key substrates such as oxygen and glucose to the fetus. Altered substrate availability (e.g. decreased acetyl Co-A, or S-Adenosyl methionine) can directly influence epigenetic mediators resulting in epigenetic modifcations of key genes. Decreased levels of glucose and oxygen can also impair mitochondrial function and increase production of ROS. These processes can have a detrimental affect on numerous cellular pathways culminating in fetal programming.