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Nutrient Sensor Mediated Programmed Non-Alcoholic Fatty Liver Disease in Low Birth Weight Offspring
American Journal of Obstetrics and Gynecology, 08/08/2012
Wolfe D et al. – These findings suggest that undernutrition stress in utero may program hepatic nutrient sensors to perceive normal postnatal nutrition as a state of nutrient excess with induction of hepatic lipid storage.
Methods- Pregnant dams received ad libitum food or were 50% food restricted from pregnancy day 10 to 21 to produce Control and LBW newborns, respectively.
- All pups were nursed by control dams and weaned to ad libitum feed.
- They determined hepatic SIRT1 (NAD+–dependent histone deacetylase) and AMPK (AMP–activated protein kinase) activities, and protein expression of lipid targets in LBW and Control fetuses (e20), newborns (p1) and adults (3 months).
- LBW fetuses demonstrate increased prenatal hepatic SIRT1 activity though with increased lipogenesis.
- Following birth, LBW undergo postnatal suppression of hepatic SIRT1 and AMPK activities in conjunction with increased lipogenesis, decreased lipolysis and increased fat stores.
