Nutrient sensor–mediated programmed nonalcoholic fatty liver disease in low birthweight offspring
D Wolfe, M Gong, G Han, TR Magee, MG Ross… - American journal of …, 2012 - Elsevier
OBJECTIVE: We hypothesized that gestationally programmed nonalcoholic fatty liver
disease in low-birthweight offspring is mediated through nutrient sensors nicotinamide
adenine dinucleotide+–dependent histone deacetylase (SIRT1) and AMP-activated protein
kinase (AMPK). STUDY DESIGN: Pregnant dams received ad libitum food or were 50% food
restricted from pregnancy days 10-21 to produce control and low-birthweight newborn
offspring, respectively. All pups were nursed by control dams and weaned to ad libitum feed …
disease in low-birthweight offspring is mediated through nutrient sensors nicotinamide
adenine dinucleotide+–dependent histone deacetylase (SIRT1) and AMP-activated protein
kinase (AMPK). STUDY DESIGN: Pregnant dams received ad libitum food or were 50% food
restricted from pregnancy days 10-21 to produce control and low-birthweight newborn
offspring, respectively. All pups were nursed by control dams and weaned to ad libitum feed …