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. Author manuscript; available in PMC: 2014 Sep 1.
Published in final edited form as: Clin Obstet Gynecol. 2013 Sep;56(3):577–590. doi: 10.1097/GRF.0b013e3182a09760

Figure 1. In utero lipid excess and hepatocyte maladaptive changes.

Figure 1

Increased lipid flux to the developing fetal liver establishes a lipotoxic environment characterized by oxidative stress, increased inflammation, cell death, and consequent dysregulation in oxidative metabolism genes. Additionally, Kupffer cell and hepatic stellate cell (HSC) pro-inflammatory priming by hepatocellular stress as well as direct stimulation by circulating lipids may also increase susceptibility to later disease. Antioxidant enzymes (AOX), Reactive Oxidative Species (ROS), Sirtuin 1 and 3 (SIRT1 and SIRT3), Toll-like receptors (TLR).