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Early onset of fatty liver in growth-restricted rat fetuses and newborns
Makiko Yamada1, Diana Wolfe, Guang Han
1Perinatal Research Laboratories, Department of Obstetrics and Gynecology, Los Angeles Biomedical Research Institute, Harbor-UCLA Medical Center, USA.
Insights
Intrauterine growth restriction (IUGR) in rat pups leads to a "programmed" fatty liver present even before birth. This suggests IUGR alters metabolic strategies for increased fuel storage, impacting long-term health.
Area of Science:
- Developmental Biology
- Metabolic Syndrome Research
- Perinatal Medicine
Background:
- Intrauterine growth restriction (IUGR) is linked to adult metabolic syndrome, including fatty liver.
- The origin of fatty liver in IUGR (programmed vs. obesity-related) remains unclear.
Purpose of the Study:
- To investigate hepatic lipid accumulation and lipogenic factors in IUGR and control rat pups at fetal and newborn stages.
- To determine if fatty liver in IUGR is a result of gestational programming.
Main Methods:
- Examined hepatic lipid content and key lipid-regulatory factors (SREBP-1c, FAS) in IUGR and control rat fetuses (embryonic day 20) and newborns (postnatal day 1).
Main Results:
- IUGR fetuses exhibited "fatty liver" with upregulated lipogenic indices (SREBP-1c, FAS) by embryonic day 20.
- Both IUGR and control newborns showed similar massive increases in hepatic lipids, but IUGR maintained upregulated lipogenic indices.
Conclusions:
- Persistent upregulation of lipogenic factors in IUGR fetuses and newborns indicates gestational programming of fatty liver.
- IUGR offspring appear to possess an altered metabolic strategy favoring increased fuel/lipid storage, potentially a thrifty phenotype pathway.
Abstract:
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.
