The mTOR is a 289 kDa serine/threonine kinase, which plays a key role in regulating cell growth and proliferation. Moreover, 4EBP1 is phosphorylated by mTOR to regulate translation initiation, whereas Akt contributes to mTOR activation. Results showed that these proteins are significantly down-regulated after exposure to DON, indicating DON inhibits protein synthesis, consequently leading to decreased cell proliferation. Previous report showed several mycotoxins, particularly DON, causes the cell cycle arrest in the Gap2/ Metaphase phase. The G2/M arrest in intestinal epithelium cells caused by DON is associated with its inhibition on Akt/mTOR pathway because the inhibition of Akt/mTOR induces G2/M arrest in cells. The levels of these proteins are up-regulated with dietary glutamic acid supplementation. This indicated that glutamic acid contributes to protein synthesis by regulating cell cycles. Indeed, previous studies have shown that glutamic acid appears to be involved in cellular signaling and growth regulation. Taken together, our findings demonstrated that DON induces oxidative stress, and increases intestinal permeability, as well as inhibits protein synthesis and cell proliferation in weaned piglets. Glutamic acid Reversine supplementation decreases the oxidative stress and the intestinal permeability, and reverses Akt/mTOR/4EBP1 signaling caused by DON, indicating glutamic acid is a useful nutritional regulator for DON damage. Non-alcoholic fatty liver disease is a common liver disease that is characterized by hepatic steatosis. Most patients with NAFLD exhibit non-progressive simple fatty liver, namely non-alcoholic fatty liver. Non-alcoholic steatohepatitis is a more severe form of NAFLD that is characterized by lobular inflammation, hepatocellular ballooning, and fibrosis with an inherent risk for progression to cirrhosis and hepatocellular carcinoma. These features were defined by Ludwig et al. in 1980 to describe a liver disease that histologically mimics alcoholic hepatitis but occurs in individuals who do not abuse alcohol. Because NASH can progress towards end-stage liver disease requiring a liver transplant, therapies for NASH must be developed. Even though the mechanisms of the progression from simple steatosis to NASH are not completely understood, accumulating evidence suggests a major role of mitochondrial dysfunction in steatosis and steatohepatitis. Mitochondrial dysfunction not only impairs fat homeostasis in the liver but also leads to an overproduction of oxidative stress-inducing reactive oxygen species that trigger lipid peroxidation, cytokine overproduction, and cell death. Indeed, ultrastructural alterations, impairment of adenosine triphosphate synthesis, and increased production of ROS have been reported in liver mitochondria from NASH patients and a rodent model. Vitamin E supplementation, the prototypical antioxidant drug treatment, has become a standard treatment for NASH. However, most clinical studies of atherosclerotic diseases with dietary antioxidants have not generated clear results, partly because of the non-selective effects of these anti-oxidative drugs.