2 Glut-2 has been shown to be decreased, suggesting impaired metabolism of carbohydrates. All of this was associated with increased tumor necrosis
factor alpha (TNF-β), decreased hepatic mitochondrial electron transport chain enzyme complex activity, and liver inflammation in the offspring simply from high-fat diet during gestation.2–6 The roles for maternal and child dietary composition, and the potential for novel understanding of the response of nonparenchymal cells and innate immunity in liver, is explored by Mouralidarane et al.7 In their study, offspring of obese Sirolimus order mice fed a high-fat/high-sugar diet during gestation appeared to be sensitized to a postnatal obesogenic diet because they developed more severe weight gain, hypertriglyceridemia, hepatic inflammation, and fibrosis compared to those exposed either during pregnancy alone or postnatally alone. Interestingly, the dual effect of prenatal and postnatal obesogenic diets appeared to be more than additive in its effect on hepatic fat. Maternal obesity alone did not cause significant weight gain or hepatic fat in the offspring. One issue with the experimental design used by Mouralidarane et al.7 is the inability to assess if the effects are from the gestational weight gain or from the specific macronutrient change. Previous studies have shown fructose and fat have effects on offspring without gestational weight gain.2, 8 Fructose in
the water of pregnant Wistar rats induced SREBP-1c messenger RNA check details (mRNA) and protein expression and fatty acid synthase mRNA expression
in the fetal livers without significant weight gain in the dams.8 While it is difficult to separate effects of weight gain from high-fat and/or high-fructose diets during gestation, this is a potential area of future research that has important implications for public health. Another important distinction is if increased body weight, fat mass, and hepatic fat in the offspring of obese mothers was from increased consumption compared to those without obese mothers. Given the previous work demonstrating increased fat preference by offspring, it would be interesting to know if the feeding behavior was altered by the 上海皓元 maternal obesity or if the effects were transmitted through decreased tolerance of the postnatal obesogenic diet. Mouralidarane et al. also examined the role of innate immune system dysfunction. They documented increased Kupffer cells numbers, impaired phagocytic function of the Kupffer cells, and increased reactive oxygen species (ROS) production in the mice with pre- and postnatal exposure to the obesogenic diet. Decreased function of Kupffer cells is an important area of interest in the mechanism of NAFLD. Impaired clearance of lipopolysaccharide (LPS) by Kupffer cells could result in accelerated liver injury,9 as seen in the pre- and postnatal-exposed offspring.