Body Cholesterol Removal: Role of Plasma High-Density Lipoproteins1 1Supported by National Health Service Grants HL 18673, HL 07291, and HL 22682, and a Grant-In-Aid from the American Heart Association (316–3070–2286).
1980; Elsevier BV; Linguagem: Inglês
10.1016/b978-0-12-024917-6.50007-0
ISSN0065-2849
Autores Tópico(s)Cancer, Lipids, and Metabolism
ResumoThe human body is equipped with mechanisms for the provision and maintenance of tissue cholesterol levels. Cholesterol absorption increases with dietary intake, with no upper limit. In times of reduced intake, the liver and small intestine increase their synthesis of cholesterol. Absorbed cholesterol is transported to the liver as chylomicron remnants and hepatic cholesterol is either secreted as "very low-density lipoproteins," which are catabolized in part to low-density lipoproteins (LDL), or secreted into bile as free cholesterol or its metabolites, the bile salts. LDL delivers cholesterol to the peripheral tissues, where specific cell surface receptors bind, internalize, and degrade the LDL particles, providing the cell with cholesterol. In the absence of an adequate supply of lipoprotein cholesterol, the cholesterol synthesis pathway is activated in peripheral tissues. This chapter discusses the high-density lipoproteins (HDL) structure and metabolism, particularly as it might be related to cholesterol homeostasis. It focuses on the composition and structure of HDL, the physical structure of the individual components of HDL, and the different HDL recombinants.
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