Palmitate induces insulin resistance in H4IIEC3 hepatocytes through reactive oxygen species produced by mitochondria.

Visceral adiposity in obesity causes excessive free fatty acid (FFA) flux into the liver via the portal vein and may cause fatty liver disease and hepatic insulin resistance. However, because animal models of insulin resistance induced by lipid infusion or a high fat diet are complex and may be accompanied by alterations not restricted to the liver, it is difficult to determine the contribution of FFAs to hepatic insulin resistance. Therefore, we treated H4IIEC3 cells, a rat hepatocyte cell line, with a monounsaturated fatty acid (oleate) and a saturated fatty acid (palmitate) to investigate the direct and initial effects of FFAs on hepatocytes.

Tranilast, an antifibrogenic agent, ameliorates a dietary rat model of nonalcoholic steatohepatitis.

Unlabelled: Nonalcoholic steatohepatitis (NASH) is the progressive form of nonalcoholic fatty liver disease and is one of the most common liver diseases in the developed world. The histological findings of NASH are characterized by hepatic steatosis, inflammation, and fibrosis. However, an optimal treatment for NASH has not been established.

Regulation of adiponectin receptor expression in human liver and a hepatocyte cell line.

Nonalcoholic fatty liver disease (NAFLD) is closely associated with obesity. An adipocyte-derived hormone, adiponectin, may play a role in the pathophysiology of NAFLD through insulin-sensitizing and antifibrotic effects. We found that hepatic expression of adiponectin receptor AdipoR2, but not AdipoR1, was down-regulated in 14 patients with NAFLD compared with 7 patients with a normal liver (P < .