High-Density Lipoproteins: Structure, Metabolism, Function by Anatol Kontush, M. John Chapman

By Anatol Kontush, M. John Chapman

A entire consultant to the position of high-density lipoproteins (HDL) in new and rising therapies

With high-density lipoproteins (HDL) taking part in an expanding function in heart problems prevention, there's a transforming into desire for an in-depth examine HDL and its medical price. This ebook summarizes the present country of information within the box, offering for the 1st time a accomplished, systematic, stylistically coherent, and updated assessment of the composition, constitution, heterogeneity, metabolism, epidemiology, genetics, and serve as of HDL.

Divided into 3 major components, High-Density Lipoproteins first examines basic HDL debris, then describes faulty HDL, and at last addresses the healing normalization of subnormal degrees and faulty organic actions of this lipoprotein classification. The booklet highlights the practical homes of HDL, that are appropriate to the pathophysiology of atherosclerosis and thrombosis, and discusses the compositional and metabolic heterogeneity of HDL debris.

Readers will come away with a transparent realizing of the function of HDL in organic procedures, the capability worth of useful HDL as a healing objective, and the way present and rising treatments are poised to steer the therapy of middle disorder sooner or later.

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Extra info for High-Density Lipoproteins: Structure, Metabolism, Function and Therapeutics

Example text

The primary amino acid sequence of LCAT is highly conserved between species. Mature LCAT protein is synthesized from a 440-residue precursor following cleavage of a 24-residue signal peptide. The mature protein contains 416 amino acids and is heavily N-glycosylated. As a result, its molecular mass of 63 kDa is higher than predicted. The tertiary structure of LCAT is maintained by two disulfide bridges and resembles that of lipases and other proteins of the alpha/beta hydrolase fold family [85] (Fig.

Hepatic expression of SAA1 and SAA2 genes is regulated by the pro-inflammatory cytokines interleukin (IL)-1, IL-6 and tumour necrosis factor (TNF)-alpha. Expression of SAA1 and SAA2 in the liver is induced during the acute-phase reaction, resulting in an increase in their circulating levels by as much as 1000-fold from basal concentrations of about 1 to 5 mg/l [103]. In contrast, SAA4 is constitutively expressed in the liver and is, therefore, termed “constitutive SAA”. 1 of chapter 8). HDL is a major carrier of SAA1 in human, rabbit and murine plasma [105–107].

The enzyme consists of 505 amino acids, is N-glycosylated, cleaves the thioether bond of prenyl-L-cysteines, such as farnesylcysteine and geranylgeranylcysteine, and requires flavin adenine dinucleotide as a cofactor. Other minor abundance proteins reported to be associated with HDL are: albumin, alpha-1B-glycoprotein, alpha-amylase, vitamin D-binding globulin and platelet basic protein [8, 10]. Interestingly, many proteins traditionally known to be largely, or exclusively, carried by HDL are also present in LDL and VLDL isolated by density gradient ultracentrifugation.

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