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• W1024428191 abstract "Publisher Summary Etiology and treatment of atherosclerosis, hyperlipidemia, and cholelithiasis are discussed in this chapter. The inheritance of xanthomatosis and hyper-β-lipoproteinemia, the segregation pattern satisfies the criteria for autosomal dominant inheritance, but not for a polygenic trait. Defective removal of low density lipoproteins (LDL) from the circulation produce the elevated LDL and plasma cholesterol observe in Type II hyperlipoproteinemia. This defect appear is related to the decreased number of LDL receptors on the cell surfaces. Leukocytes from the subjects with familial hypercholesterolemia respond to incubation in a lipid-depleted medium with a higher activation of sterolsynthesis and an enhanced induction of HMG-CoA reductase compared to the leukocytes from controls. This increase insterol synthesis and HMGCoA reductase is correlated with a loss of cholesterol into the medium. A phospholipid-protein-cell interacion is necessary to induce the reductase. Lipoprotein lipases play a critical role in the metabolism of lipoproteins, and thus involve in atherogenesis. Hypercholesterolemia in the cholesterol-fed rabbit is attributed to the accumulation of chylomicron remnants that is formed on the aorta wall by lipoproteinlipase and deposit in the deep layers of the arterial wall without prior release into the blood stream. Arteriography provides unequivocal proof of lesion regression. A high-cholesterol, high-fat diet combined with arterial injury produced atherosclerosis in swine and monkeys. Chronic hyperlipidemia produces the primary endothilial injury that initiates the process of atherosclerosis." @default.
• W1024428191 created "2016-06-24" @default.
• W1024428191 creator A5020545141 @default.
• W1024428191 creator A5023749764 @default.
• W1024428191 creator A5082394989 @default.
• W1024428191 date "1977-01-01" @default.
• W1024428191 modified "2023-09-26" @default.
• W1024428191 title "Chapter 20. Recent Advances in the Etiology and Treatment of Disorders of Lipid Metabolism" @default.
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