Excess fructose enhances oleatic cytotoxicity via reactive oxygen species production and causes necroptosis in hepatocytes.

Non-alcoholic fatty liver disease (NAFLD), the hepatic phenotype of metabolic syndrome, has been identified as a major health concern as the number of cirrhosis and deaths associated with NAFLD is expected to increase. Although fructose intake has been considered to be a progressive factor in the pathophysiology of NAFLD, it remains unclear how fructose contributes to hepatocellular damage during lipotoxicity. In the present study, we aimed to analyze the hepatotoxicity of fructose in steatosis.

Serum alpha-fetoprotein increases prior to fibrosis resolution in a patient with acute liver failure.

A 78-year-old woman who was diagnosed with acute liver failure due to an undetermined cause presented with liver atrophy. Coagulopathy was normalized at 35 days of hospitalization, although atrophy in the liver persisted. During the observation period, alpha-fetoprotein (AFP) bi-modally increased at 36 and 377 days.

Unfavorable prognosis of patients with acute liver injury due to drug-induced liver injury and acute exacerbation of hepatitis B virus infection.

Aim: Acute liver injury (ALI) has a favorable prognosis, whereas acute liver failure (ALF) leads to organ failure and thus has an unfavorable prognosis. The effect of each etiology on the clinical course of ALI remains unclear. This study aimed to determine how each etiology and glucocorticoid on the unfavorable etiology affects the clinical course of ALI.

Caspase-independent hepatocyte death: A result of the decrease of lysophosphatidylcholine acyltransferase 3 in non-alcoholic steatohepatitis.

Background And Aims: Lipotoxicity causes liver inflammation, which leads to non-alcoholic steatohepatitis (NASH). Lysophosphatidylcholine (LPC) is a causal agent of lipotoxicity. Recently, lysophosphatidylcholine acyltransferase (LPCAT) was identified as an enzyme that catalyzes the esterification of LPC, which potentially decreases LPC levels.