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: A recent study showed improvement in insulin sensitivity with the use of venesection in patients with NAFLD, but this approach cannot be implemented without extensive review.

TL;DR: It is concluded that only some histologic features previously reported in NAFLD (especially those with substantial and moderate concordance for both interobserver and intraobserver interpretation) are interpreted uniformly by experienced pathologists.

TL;DR: High resolution two-dimensional gel electrophoresis of livers showed that WY14,643 and rosiglitazone both produced changes in expression pattern of many proteins involved in peroxisomal fatty acid beta-oxidation, however, similar experiments performed in lean mice showed significant up-regulation of these proteins only with WY 14,643 treatment.

TL;DR: It is shown that phosphorylated Cbl recruits the CrkII–C3G complex to lipid rafts, where C3G specifically activates the small GTP-binding protein TC10, which is essential for insulin-stimulated glucose uptake and GLUT4 translocation.