Early onset of fatty liver in growth-restricted rat fetuses and newborns
Article first published online: 21 NOV 2011
© 2011 The Authors. Congenital Anomalies © 2011 Japanese Teratology Society
Volume 51, Issue 4, pages 167–173, December 2011
How to Cite
Yamada, M., Wolfe, D., Han, G., French, S. W., Ross, M. G. and Desai, M. (2011), Early onset of fatty liver in growth-restricted rat fetuses and newborns. Congenital Anomalies, 51: 167–173. doi: 10.1111/j.1741-4520.2011.00336.x
- Issue published online: 21 NOV 2011
- Article first published online: 21 NOV 2011
- Accepted manuscript online: 8 SEP 2011 10:55AM EST
- Received August 8, 2011; revised and accepted September 5, 2011.
- fatty acid synthase;
- fatty liver;
- intrauterine growth retardation;
- sterol regulatory element-binding protein 1
Intrauterine growth-restricted (IUGR) newborns have increased risk of adult metabolic syndrome, including fatty liver. However, it is unclear whether the fatty liver development is “programmed” or secondary to the accompanying obesity. In this study, we examined hepatic lipid accumulation and lipid-regulatory factors (sterol regulatory element-binding protein-1c and fatty acid synthase) in IUGR and Control fetal (embryonic day 20; e20) and newborn (postnatal day 1; p1) rat pups. Notably, despite of in utero undernutrition state, IUGR fetuses demonstrated “fatty liver” with upregulation of these lipogenic indices at as early as e20. Both IUGR and Control newborns exhibited the same extent of massive increase in hepatic lipid content, whereas IUGR newborns continued to exhibit upregulated lipogenic indices. The persistent upregulation of the lipogenic indices in fetal and newborn IUGR suggests that fatty liver is gestationally programmed. Our study suggested that IUGR offspring were born with an altered metabolic life strategy of increased fuel/lipid storage which could be a distinct metabolic pathway of the thrifty phenotype.