Figure 2. Evidence of fetal programming in human mesenchymal stem cells.

Human mesenchymal stem cells (MSCs), progenitors to hepatic stellate cells (HSCs), demonstrate evidence of fetal programming in relation to maternal obesity, maternal circulating lipids, and neonatal adiposity and adiposity gain over time. These cells have exhibited lipid transport and accumulation, incomplete β-oxidation, increased anaplerosis, and diminished ETC activity. Oxidative stress is coupled with increased GSH metabolism, and gene expression indicates alterations in nutrient sensing along with increased apoptotic and inflammatory signaling. OMM, outer mitochondrial membrane; IMM, inner mitochondrial membrane; CACT, carnitine-acylcarnitine translocase; DCAC, dicarboxylic acylcarnitines.