ArticleHepatology (Baltimore, Md.)2013
Homeostatic generation of reactive oxygen species protects the zebrafish liver from steatosis.
Article in Hepatology (Baltimore, Md.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 31 citations in OpenAlex.
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- Three-dimensional structural analysis reveals a Cdk5-mediated kinase cascade regulating hepatic biliary network branching in zebrafish.Development (Cambridge, England) · 2017Article
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- The raspberry Gene Is Involved in the Regulation of the Cellular Immune Response in Drosophila melanogaster.PloS one · 2016Article
- Zebrafish: an important tool for liver disease research.Gastroenterology · 2015Review
- Strategies, models and biomarkers in experimental non-alcoholic fatty liver disease research.Progress in lipid research · 2015Review
- Aldehyde dedydrogenase-2 plays a beneficial role in ameliorating chronic alcohol-induced hepatic steatosis and inflammation through regulation of autophagy.Journal of hepatology · 2015Article
- ROS: redux and paradox in fatty liver disease.Hepatology (Baltimore, Md.) · 2013Article
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7 authors at 2 institutions in 1 country.
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Abstract
unlabelledNonalcoholic fatty liver disease is the most common liver disease in both adults and children. The earliest stage of this disease is hepatic steatosis, in which triglycerides are deposited as cytoplasmic lipid droplets in hepatocytes. Through a forward genetic approach in zebrafish, we found that guanosine monophosphate (GMP) synthetase mutant larvae develop hepatic steatosis. We further demonstrate that activity of the small GTPase Rac1 and Rac1-mediated production of reactive oxygen species (ROS) are down-regulated in GMP synthetase mutant larvae. Inhibition of Rac1 activity or ROS production in wild-type larvae by small molecule inhibitors was sufficient to induce hepatic steatosis. More conclusively, treating larvae with hydrogen peroxide, a diffusible ROS that has been implicated as a signaling molecule, alleviated hepatic steatosis in both GMP synthetase mutant and Rac1 inhibitor-treated larvae, indicating that homeostatic production of ROS is required to prevent hepatic steatosis. We further found that ROS positively regulate the expression of the triglyceride hydrolase gene, which is responsible for the mobilization of stored triglycerides in hepatocytes. Consistently, inhibition of triglyceride hydrolase activity in wild-type larvae by a small molecule inhibitor was sufficient to induce hepatic steatosis.
conclusionDe novo GMP synthesis influences the activation of the small GTPase Rac1, which controls hepatic lipid dynamics through ROS-mediated regulation of triglyceride hydrolase expression in hepatocytes.
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