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Multiple mechanisms have proposed to explain the accumulation of TG in the liver, including (i) increased dietary fat intake, (ii) excess free fatty acid (FFA) delivery from lipolysis of white adipose tissue, (iii) increased de novo lipogenesis, (iv) reduced fatty acid -oxidation, and (v) reduced fat export in the form of very low-density lipoprotein (VLDL) ( de novo fatty acid and cholesterol synthesis ( Two-Hit or Multiple-Hit Hypothesis Steatosis can prime the liver to develop more progressive liver pathologies in response to additional metabolic and/or environmental stressors

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This paper is a cross-institution collaborative project from the Toxicity Special Interest Group supported, in part, by the Center for Coordination of Analytics, Science, Enhancement and Logistics (CASEL) in Tobacco Regulatory Science (TRS), U54DA046060 (National Institute of Drug Abuse (NIDA), and the U.S

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