<s>[INST] context: Free fatty acids are normally taken up by the liver and esterified to triglyceride, conveed to cholesterol, oxidized into ketone bodies, or incorporated into phospholipids that can be excreted from the liver as very-low-density lipoproteins (VLDLs). Abnormalities involving any of these normal metabolic pathways may lead to the accumulation of triglycerides within the hepatocytes. This accumulation of triglycerides is called fatty change or steatosis. Examples of abnormalities that produce hepatic steatosis include diseases that cause excess delivery of free fatty acids to the liver or diseases that cause impaired lipoprotein synthesis. Excess delivery of free fatty acids occurs in conditions that increase lipolysis of adipose tissue, such as starvation, diabetes mellitus, and coicosteroid use. Increased formation of triglycerides can result from alcohol use, as alcohol causes excess NADH formation (high NADH/NAD ratio), increases fatty acid synthesis, and decreases fatty acid oxidation. Impaired apoprotein synthesis occurs with carbon tetrachloride poisoning, phosphorous poisoning, and protein malnutrition. Inhibition of HMG-CoA reductase activity is the mechanism of lovastatin, which indirectly increases liver LDL receptors and increases LDL clearance from the blood. [/INST] question: Increased lipolysis of fat stores, which can result from starvation, diabetesmellitus, or coicosteroid use, is most likely to cause steatosis (fattyliver) through which one of the listed mechanisms? | options: A: Decreased free fatty acid excretion from the liver leads to free fatty acid accumulation in hepatocytes B: Excess NADH (high NADH/NAD ratio) causes excess production of lactate from pyruvate, which accumulates in hepatocytes C: Increased free fatty acid delivery to the liver leads to triglyceride accumulation in hepatocytes D: Inhibition of apoprotein synthesis by the liver leads to phospholipid accumulation in hepatocytes | answer: C </s>