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Blocked production and secretion of lipoproteins is often the main cause of triglyceride accumulation in the liver. Impaired apolipoprotein synthesis is the most important pathogenetic factor in several types of toxic fatty liver and in the fatty liver produced by protein-calorie malnutrition. Toxic inhibition of protein synthesis can lead to a fatty liver through inhibition of mRNA synthesis or translation. In microvesicular 'liver failure' fatty liver, small droplets of triglyceride plus FFA, cholesterol, and phospholipid collect 'liver failure' in subcellular organelles. The basic defect is unknown, even though pathologic and clinical features from diverse causes are somewhat similar. The biochemical basis may be a disturbance in the mitochondrial-oxidative pathway, depressing FFA oxidation and impairing apolipoprotein synthesis for VLDL assembly.
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