Jim Yan

TL;DR: It is found that MCD feeding causes profound hepatic suppression of the gene encoding stearoyl-coenzyme A desaturase-1 (SCD-1) in the liver, which likely contributes to hypermetabolism and weight loss.

TL;DR: It is concluded that APP protects neuronal cells against apoptosis by controlling p53 activation at the post-translational level and disruption of this function by mutations or alterations in APP processing could enhance neuronal vulnerability to secondary insults and contribute to neuronal degeneration.

TL;DR: Results indicate that dietary sucrose is critical to the pathogenesis of MCD-mediated steatohepatitis and suggest that saturated fatty acids, which are products of de novo lipogenesis, are mediators of hepatic toxicity in this model of liver disease.

TL;DR: Results indicate that dietary PUFAs promote hepatic inflammation but not hepatotoxicity in the MCD model of liver disease, and emphasize that individual dietary nutrients can make specific contributions to steatohepatitis.

TL;DR: MCD feeding causes an integrated stress response in the liver rather than a classic unfolded protein response, and CHOP, despite its identity as a mediator of stress-related cell death, does not play a central role in the pathogenesis of MCD-mediated liver disease.