Fructose leads to hepatic steatosis in zebrafish that is reversed by mechanistic target of rapamycin (mTOR) inhibition.

@article{Sapp2014FructoseLT,
  title={Fructose leads to hepatic steatosis in zebrafish that is reversed by mechanistic target of rapamycin (mTOR) inhibition.},
  author={Valerie Sapp and Leah P Gaffney and Steven F Eauclaire and Randolph P. Matthews},
  journal={Hepatology},
  year={2014},
  volume={60 5},
  pages={1581-92}
}
UNLABELLED Nonalcoholic fatty liver disease (NAFLD), the accumulation of lipid within hepatocytes, is increasing in prevalence. Increasing fructose consumption correlates with this increased prevalence, and rodent studies directly support fructose leading to NAFLD. The mechanisms of NAFLD and in particular fructose-induced lipid accumulation remain unclear, although there is evidence for a role for endoplasmic reticulum (ER) stress and oxidative stress. We have evidence that NAFLD models… CONTINUE READING
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