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Most triglycerides enter an active pool where they combine with specific apoproteins to form lipoproteins (eg, very low density lipoproteins [VLDLs]), which are secreted into plasma. The liver is also responsible for lipid degradation (eg, low density lipoproteins, chylomicron remnants). Fatty liver occurs when lipid accumulation exceeds the normal 5% of liver weight. In the macrovesicular type, large fat white girls fat droplets balloon the liver cell, displacing the nucleus to the fat white girls periphery of the cell, like an adipocyte. Triglyceride accumulates most commonly because it has the highest turnover rate of all hepatic fatty acid esters. Liver fat white girls uptake of FFA from adipose tissue and the diet is unrestrained, whereas FFA disposition by oxidation, esterification, and VLDL secretion is limited. In microvesicular fatty liver, small fat droplets accumulate, cells appear foamy, and nuclei are central. Triglycerides collect in subcellular organelles (eg, endoplasmic reticulum), reflecting widespread metabolic disturbance.
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