High-fat feeding in mice resulting in increased body weight and hepatic steatosis causes selective natural killer T (NKT) cell depletion in the liver and is associated with increased production of proinflammatory cytokines such as TNF-β and interferon-gamma

(IFN-γ).6 This is consistent with the findings of Mouralidarane et al., which again demonstrated a decrease in NKT cells in the liver in response to a postnatal high-fat/high-sugar diet. They add to the picture by demonstrating further depletion in the combined group compared with postnatal Erlotinib concentration exposure alone. In conclusion, this article and others demonstrate a powerful influence of maternal obesity and a gestational obesogenic diet to sensitize the offspring to induction of NAFLD. This multiplicative Ponatinib effect is important because it could help explain the rapid rise in pediatric NAFLD. Further,

the combination of pre- and postnatal exposure to the diet resulted in a nonalcoholic steatohepatitis (NASH)-like picture, with increased profibrogenic markers, increased fibrosis in the liver, and increased inflammation associated with alterations in innate immunity. This has particular relevance to the consideration of why some children have severe features of NASH at relatively young ages. The findings lend support for carefully designed human studies, particularly for populations known to be at high risk for NAFLD. “
“Characterization of key cellular and molecular mechanisms responsible for efficient liver regeneration in response to acute loss of liver mass has been an active area of investigation for the past several decades.1 The intriguing search for the molecular identity of one or more factors responsible for liver regeneration has contributed substantially to our current knowledge of the functional significance Sclareol of key humoral factors and temporal events necessary for efficient liver regeneration. Several early events associated with liver regeneration have been attributed to acute hemodynamic changes and associated shear-stress–induced release of humoral factors such as nucleotides and nitric oxide from the hepatic parenchyma.2-6

Cytokine-mediated and growth factor–mediated induction of cell signaling has been shown to be integral to the activation of a highly orchestrated gene expression program responsible for the stepwise reorganization of extracellular matrix, cell proliferation, and liver growth.1 fld, fatty liver dystrophy. Studies based on 70% partial hepatectomy of rodents, especially in gene knockout and transgenic mice, have uncovered the functional significance of distinct signaling cascades and genes necessary for cell proliferation and survival in regenerating livers. However, despite distinct delays and profound impairments in hepatocyte proliferation seen in most experimental models, liver growth continues until the optimal ratio of liver weight to body weight—a species-specific set point—is reached.