Inhibiting triglyceride synthesis improves hepatic steatosis but exacerbates liver damage and fibrosis in obese mice with nonalcoholic steatohepatitis

By K. Yamaguchi, Liu Yang, S. McCall, Jiawen Huang, Xing Yu, S. Pandey, S. Bhanot, B. Monia, Yin-xiong Li, A. Diehl. Hepatology, 2007

1,024 citations recorded by the source corpus.

Subfields: Biochemistry, Epidemiology, Hepatology

View Paper: https://www.semanticscholar.org/paper/b4fa22e51f6a134f06519d3ff8e08d8430e5a044

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Citations in the corpus

Pathogenesis of non-alcoholic fatty liver disease (2009, methodology): “There is now substantial evidence that FFA can directly cause toxicity by increasing oxidative stress and by activation of inflammatory pathways,(26) therefore hepatic triglyceride accumulation may be a protective mechanism by preventing the toxic effects of unesterified FFA.(27) Additionally, a fur”
NAFLD: a multisystem disease. (2015, background): “Journal of Hepatology 201 products (particularly DAGs) is very important in causing ‘resistance’ within the hepatic insulin signaling pathway [61], promoting hepatic inflammation [62–65] and increasing risk of progressive liver disease that occurs with NASH.”
The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “Triglyceride accumulation is not hepatotoxic per se and could represent a defensive mechanism to balance FFAs excess as demonstrated inmicemodels [19,20].”
Lipotoxicity and the gut-liver axis in NASH pathogenesis. (2018, background): “[13] demonstrated that blocking triglyceride synthesis via inhibition of diacylglycerol acyltransferase 2 results in a reduction of steatosis, associated with increased oxidative stress, inflammation, and fibrosis.”
The interaction of hepatic lipid and glucose metabolism in liver diseases. (2012, background): “As mentioned above, lysosomes process chylomicron remnants as well as TAGs that accumulate during hepatic lipogen- 956 Journal of Hepatology 201 esis.”
Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease (2018, background): “In this study, despite a reduction of hepatic steatosis, it showed an increase of lipid oxidant stress markers and a worsening of lobular necroinflammation and fibrosis compared to controls, suggesting that steatosis may be a protective mechanism to prevent the progression of liver damage in NAFLD [”
Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “The accumulation of triglyceride as lipid droplets in NASH is orchestrated by a complex array of facilitating proteins(125) and factors that impair this process, predisposing to lipotoxic injury and defects in insulin signaling in cell culture(23,28,126) and in animal studies.(22,54,127,128) Corrobo”