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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Lipoprotein lipase activator ameliorates the severity of dietary steatohepatitis.

Dietary model of steatohepatitis was established by feeding mice a methionine choline deficient (MCD) diet. Mice on MCD or control diet for 3 weeks were treated with or without NO-1886, a newly synthetic lipoprotein lipase ( LPL) activator. In a separate experiment, NO-1886 was given after pre-treatment with 3 weeks of MCD diet. NO-1886 significantly reduced MCD-induced inflammation by repressing levels of hepatic lipid peroxides and pro-inflammatory tumor necrosis factor-alpha ( TNF-alpha), interleukin-6 ( IL-6), and cyclooxygenase-2 ( COX-2). In addition, NO-1886 dampened hepatic steatosis via accelerating fatty acid oxidation caused by enhanced expression of PPARalpha, cytochrome P450-10 (Cyp4a10), and Acyl-CoA oxidase (ACO). It failed to regulate genes of fatty acid uptake and synthesis pathways. In conclusion, NO-1886 ameliorated and induced regression of experimental steatohepatitis via increasing endogenous LPL activation resulting in suppression on pro-inflammatory factors and reduction of hepatic fatty acids. These findings indicate that NO-1886 is a potential therapeutic agent for steatohepatitis.[1]


  1. Lipoprotein lipase activator ameliorates the severity of dietary steatohepatitis. Yu, J., Chu, E.S., Hui, A.Y., Cheung, K.F., Chan, H.L., Leung, W.K., Farrell, G.C., Sung, J.J. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
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