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Increased hdl cholesterol uptake of fatty acids by hepatocytes leads to mitochondrial -oxidation overload, with the consequent accumulation of fatty acids within hdl cholesterol hepatocytes. Hyperinsulinemia resulting from insulin resistance increases the synthesis of fatty acids in hepatocytes by increasing glycolysis and favors the accumulation of triglycerides within hepatocytes by hdl cholesterol decreasing hepatic production of apolipoprotein B-10017. Since weight reduction leads to decrease in TNF-a and other factors it may improve the liver disease. As regards the cause of extracellular matrix deposition in liver tissue, the hepatic sinusoidal lumens are narrowed by swollen hepatocytes containing fat droplets and abundant enlarged endoplasmic reticula in their cytoplasm, and the hepatic sinusoidal microcirculation is impaired. Consequently, ischemia occurs in the perivenular or intralobular spaces, and hepatic fibrogenesis appears to be enhanced by ischemia, which may lead to liver cirrhosis16.
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