Regulation of Low Density Lipoprotein Receptor-related Protein Gene Expression & Cholesteryl Ester Transfer Protein-mediated HDL Selective Uptake in the Liver PDF Download
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Author: André Gauthier
Publisher:
ISBN:
Category : Cholesterol
Languages : en
Pages : 344
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Book Description
Author: André Gauthier
Publisher:
ISBN:
Category : Cholesterol
Languages : en
Pages : 344
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Book Description
Author: André Gauthier
Publisher:
ISBN:
Category : Cholesterol
Languages : en
Pages : 0
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Book Description
Author: N Myant
Publisher: Elsevier
ISBN: 0323148875
Category : Science
Languages : en
Pages : 480
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Book Description
Cholesterol Metabolism, LDL, and the LDL Receptor focuses on the cholesterol biochemistry and lipoprotein metabolism. This book is organized into 10 chapters that describe the coordinated actions of three regulated processes, namely, the intracellular synthesis of cholesterol, its esterification by ACAT, and the receptor-mediated uptake of low-density lipoprotein (LDL), for optimal level of free cholesterol. The first five chapters explore the various aspects of cholesterol biology, including discussions on the interaction of ligands with their cell-surface receptors; the role of coated pits in the endocytosis of receptor-bound ligands; and the recycling of receptors through the interior of the cell. These chapters also examine the regulation of gene expression encoding inducible proteins and the use of natural and synthetic mutations in studies of the functions of the separate domains of a multifunctional protein. A chapter describes the cloning of the apoB gene, the receptor-binding domain of apoB-100, and the unusual mode of derivation of apoB-48. Considerable chapters are devoted to LDL receptor and its pathway. The concluding chapter deals with the clinical consequences of genetic dysfunction of the LDL receptor, with particular emphasis on the diagnostic and treatment approaches of familial hypercholesterolemia that are based wholly or in part on knowledge of the LDL receptor or its gene. This book is an indispensable guide for biologists, physiologists, and clinicians who are interested in the epidemiological field of cholesterol and heart attacks.
Author: Arnold von Eckardstein
Publisher: Springer
ISBN: 9783319096643
Category : Medical
Languages : en
Pages : 0
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Book Description
In this Handbook of Experimental Pharmacology on “High Density Lipoproteins – from biological understanding to clinical exploitation” contributing authors (members of COST Action BM0904/HDLnet) summarize in more than 20 chapters our current knowledge on the structure, function, metabolism and regulation of HDL in health and several diseases as well as the status of past and ongoing attempts of therapeutic exploitation. The book is of interest to researchers in academia and industry focusing on lipoprotein metabolism, cardiovascular diseases and immunology as well as clinical pharmacologists, cardiologists, diabetologists, nephrologists and other clinicians interested in metabolic or inflammatory diseases.
Author: Christopher J. Fielding
Publisher: John Wiley & Sons
ISBN: 9783527625185
Category : Science
Languages : en
Pages : 553
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Book Description
This book meets the long-awaited need for a comprehensive overview of the biological role of HDLs. Edited by one of the pioneers in HDL and cholesterol research, this monograph summarizes current knowledge on HDL turnover, regulation and physiology. Clearly structured, the various sections cover HDL structure, formation, secretion and removal, as well as plasma metabolic factors. The biological activities and clinical aspects are equally discussed, as is the impact of HDL on common diseases and their prevention.
Author:
Publisher:
ISBN:
Category : Coronary heart disease
Languages : en
Pages : 2
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Book Description
Author: Jean-Pierre Montmayeur
Publisher: CRC Press
ISBN: 1420067761
Category : Medical
Languages : en
Pages : 646
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Book Description
Presents the State-of-the-Art in Fat Taste TransductionA bite of cheese, a few potato chips, a delectable piece of bacon - a small taste of high-fat foods often draws you back for more. But why are fatty foods so appealing? Why do we crave them? Fat Detection: Taste, Texture, and Post Ingestive Effects covers the many factors responsible for the se
Author: Kiki Chu
Publisher:
ISBN:
Category :
Languages : en
Pages : 174
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Book Description
Author: Samuel Lee
Publisher:
ISBN:
Category :
Languages : en
Pages :
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Book Description
We demonstrate that mice with liver-specific triple FoxO knockout (L-FoxO1,3,4) have increased HDL-cholesterol (HDL-C), associated with decreased expression of HDL-C clearance factors, scavenger receptor class B type I (SR-BI) and hepatic lipase, and defective selective uptake of HDL-cholesteryl ester by the liver. As such, we uncover a novel mechanism by which HDL-mediated reverse cholesterol transport to the liver is regulated by the hepatic insulin-->FoxO signaling pathway.
Author: Monika ‡e author Sharma
Publisher:
ISBN:
Category :
Languages : en
Pages : 200
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Book Description
Lipoprotein(a) (Lp(a)) comprises a low density lipoprotein (LDL) particle with one molecule of apolipoprotein B-100 (apoB-100) and one molecule of apolipoprotein(a) [apo(a)], a protein evolutionary derived from plasminogen. The apo(a) protein consists of two plasminogen kringle domains, kringle IV (KIV) and kringle V (KV). KIV is further divided into 10 subclasses, KIV1-10. Repetition of the KIV2 domain is responsible for the size heterogeneity of apo(a) isoforms. The size of apo(a) isoforms is inversely correlated with plasma Lp(a) levels and elevated levels of Lp(a) (>50 mg/dL) are directly associated with cardiovascular disease risk. Plasma Lp(a) levels and cardiovascular disease risk share a “J” shape relationship where lower plasma Lp(a) levels (50 mg/dL) reduces cardiovascular disease risk compared to those with no Lp(a). However, a proportional increase in cardiovascular disease risk is observed with increasing plasma Lp(a) levels (50 mg/dL). The beneficial effects of having low Lp(a) concentrations occur through an unknown mechanism. A significant positive correlation between Lp(a) and high density lipoprotein cholesterol (HDL-C) is observed in African-American populations and in the multi-ethnic Dallas heart study population, indicative of a biological connection between Lp(a) and HDL-C. Previous studies by our group and by others have also suggested that there is a positive connection between Lp(a) and HDL-C where elevated HDL-C levels were observed in Lp(a) transgenic mice. The first aim of this thesis was to investigate the mechanism responsible for the biological connection between Lp(a) and HDL-C. Plasma HDL-C levels are regulated by the expression of several genes in the liver. The HDL biogenesis pathway is primarily regulated by the ATP-binding cassette A1 (ABCA1), a cholesterol transporter. In this study, the effects of Lp(a) on the HDL biogenesis pathway in a hepatic cellular model (HepG2 cells) were investigated. Interestingly, Lp(a) upregulated ABCA1-mediated cholesterol efflux via the peroxisomal proliferator activated receptor and liver X receptor transcription factors. Further investigations revealed that it was the oxidised phospholipid content of Lp(a) that induced ABCA1 expression. Oxidised phospholipids from Lp(a) were delivered via the scavenger receptor-B1 (SR-B1) to stimulate an ABCA1 response in HepG2 cells. An interesting observation from these results was the internalisation of apo(a), independent of the SR-B1-mediated Lp(a) lipid internalisation. Multiple studies have implicated several receptors in Lp(a) uptake, however the precise receptor and mechanism responsible for Lp(a) clearance from plasma remains unknown. The second aim of this thesis was to characterise the uptake and intracellular trafficking of Lp(a) in HepG2 cells. This study has determined that the endocytosed Lp(a) follows an early endosome to trans-Golgi/recycling endosome trafficking route. This retrograde trafficking of Lp(a) recycles apo(a) into the media where it appears to re-assemble Lp(a). Interestingly, Lp(a) uptake was dependent on L-type calcium channels, suggesting calcium-dependent endocytosis in HepG2 cells. Notably, Lp(a) uptake was independent of proposed Lp(a) receptors, the asialoglycoprotein receptor and the LDL receptor. A preliminary investigation has revealed that the plasminogen receptor, PlgRKT might be responsible for Lp(a) internalisation. After establishing the methods to investigate the HDL synthesis pathway, the effects of chemotherapy drugs on lipid metabolism targets were investigated. This work was motivated by the findings of a colleague of my supervisor who had observed a decrease in HDL-C levels in breast cancer patients undergoing chemotherapy. This lead to the third aim: to investigate the effects of chemotherapy drugs (doxorubicin, cyclophosphamide and paclitaxel) on the HDL biogenesis pathway. Surprisingly, doxorubicin, a common chemotherapy agent, lowered HDL-C in HepG2 cells by decreasing ABCA1-mediated cholesterol efflux. Additionally, paclitaxel (another common chemotherapy agent) increased LDL-C by reducing LDLR protein levels and by stimulating the production of the apoB-containing lipoprotein particles in HepG2 cells. Another drug, cyclophosphamide, did not have any effect on lipid metabolism, indicating drug-specific effects on the HDL and LDL production pathway exist. In conclusion, this PhD thesis has progressed our understanding of Lp(a) metabolism. A potential mechanistic basis for the positive association between Lp(a) and HDL was determined. The intracellular trafficking of Lp(a) in the liver has been shown for the first time to follow a retrograde trafficking and recycling pathway of apo(a). Lp(a) uptake has been shown to be mediated by the plasminogen receptor, PlgRKT. These new findings of the catabolic fate of Lp(a) in the liver may help in tailoring therapeutics to lower plasma Lp(a) levels.
