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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]

References

  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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