Nonalcoholic Fatty Liver Disease

TL;DR: Data suggest that saturated fatty acids may represent an intrinsic second hit to the liver that hastens the development of NASH.

TL;DR: The effect of obesity on free fatty acid levels, fatty acid transport proteins (FATPs) and on extrinsic and intrinsic activation of apoptosis in the liver is studied.

TL;DR: There is no definite noninvasive test that helps to predict liver fibrosis however AST, ALT levels and AST: ALT ratio may help to determine the fibrosis in patients of NASH with diabetes in majority of cases.

TL;DR: It is suggested that a deficiency of IVA-PLA2 alleviates fatty liver damage caused by high-fat diets, probably because of the lower generation of IV a phospholipase A2 metabolites, such as prostaglandin E2.

TL;DR: The data suggest that SCD changes membrane organization and depletes a specific pool of membrane cholesterol supporting ABCA1-mediated efflux, whereas increasing availability of cholesterol for passive efflux by HDL2 may be uncoupled in pathological states associated with high SCD activity.

TL;DR: A review examines the mechanisms of growth factor-induced generation of ROS and their roles in specific receptor tyrosine kinase signaling pathways and suggests that reactive oxygen species (ROS) such as O(2).- and H( 2)O(2) function as mitogenic mediators of activated growth-factor receptor signaling.

TL;DR: Three categories of highly active antiretroviral therapy (HAART)associated major toxic effects have been identified: nucleoside‐related toxic effects, metabolic complications, and bone disease, which have broad implications on long‐term patient management.

TL;DR: Because of the destructive but asymptomatic lesion in this infant’s liver, liver function should be carefully investigated in all children with abetalipoproteinemia and chemical signs of liver dysfunction persist, particularly if diet manipulation is contemplated.