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Biochemistry of lipids, lipoproteins and membranes / edited by Neale Ridgway and Roger McLeod.

Biochemistry of Lipids: Lipoproteins and Membranes, Volume Six, contains concise chapters that cover a wide spectrum of topics in the field of lipid biochemistry and cell biology. It provides an important bridge between broad-based biochemistry textbooks and more technical research publications, off...

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Bibliographic Details
Online Access: Full Text (via ScienceDirect)
Other Authors: Ridgway, Neale (Editor), McLeod, Roger (Editor)
Format: eBook
Language:English
Published: Amsterdam : Elsevier, 2016.
Edition:Sixth edition.
Subjects:
Lipids > Metabolism.
Lipoproteins > Metabolism.
Membrane lipids > Metabolism.
Cellular signal transduction.
Table of Contents:
  • Front Cover; Biochemistry of Lipids, Lipoproteins and Membranes; Copyright; Contents; Contributors; Preface; Chapter 1
  • Functional Roles of Lipids in Membranes; 1. INTRODUCTION AND OVERVIEW; 2. DIVERSITY IN LIPID STRUCTURE; 3. PROPERTIES OF LIPIDS IN SOLUTION; 4. ENGINEERING OF MEMBRANE LIPID COMPOSITION; 5. ROLE OF LIPIDS IN CELL FUNCTION; 6. SUMMARY AND FUTURE DIRECTIONS; REFERENCES; Chapter 2
  • Approaches to Lipid Analysis; 1. INTRODUCTION AND OVERVIEW; 2. LIPID DIVERSITY; 3. CHROMATOGRAPHIC-BASED ANALYSIS OF LIPIDS; 4. BASIC CONCEPTS OF ANALYTICAL BIOCHEMISTRY; 5. LIPID MASS SPECTROMETRY.
  • 6. FUTURE DIRECTIONSREFERENCES; Chapter 3
  • Fatty Acid and Phospholipid Biosynthesis in Prokaryotes; 1. OVERVIEW OF BACTERIAL LIPID METABOLISM; 2. MEMBRANE SYSTEMS OF BACTERIA; 3. THE INITIATION MODULE; 4. THE ELONGATION MODULE; 5. THE ACYLTRANSFER MODULE; 6. THE PHOSPHOLIPID MODULE; 7. GENETIC REGULATION OF LIPID METABOLISM; 8. FUTURE DIRECTIONS; REFERENCES; Chapter 4
  • Lipid Metabolism in Plants; 1. INTRODUCTION; 2. PLANT LIPID GEOGRAPHY; 3. ACYL-ACYL CARRIER PROTEIN SYNTHESIS IN PLANTS; 4. ACETYL-COENZYME A CARBOXYLASE AND CONTROL OF FATTY ACID SYNTHESIS.
  • 5. PHOSPHATIDIC ACID SYNTHESIS OCCURS VIA PROKARYOTIC AND EUKARYOTIC ACYLTRANSFERASES6. MEMBRANE GLYCEROLIPID SYNTHESIS; 7. LIPID STORAGE IN PLANTS; 8. PROTECTIVE LIPIDS: CUTIN, WAXES, SUBERIN AND SPOROPOLLENIN; 9. SPHINGOLIPID BIOSYNTHESIS; 10. OXYLIPINS AS PLANT HORMONES; 11. STEROL AND ISOPRENOID BIOSYNTHESIS; 12. FUTURE PROSPECTS; ACKNOWLEDGEMENTS; REFERENCES; Chapter 5
  • Fatty Acid Handling in Mammalian Cells; 1. INTRODUCTION; 2. FATTY ACID BIOSYNTHESIS; 3. FATTY ACID UPTAKE, ACTIVATION AND TRAFFICKING; 4. FATTY ACID STORAGE AS TRIACYLGLYCEROL IN LIPID DROPLETS.
  • 5. FATTY ACID USE FOR ENERGY6. FATTY ACIDS AND SIGNALLING; 7. FATTY ACIDS AND DISEASE PATHOGENESIS; 8. FUTURE DIRECTIONS; REFERENCES; Chapter 6
  • Fatty Acid Desaturation and Elongation in Mammals; 1. INTRODUCTION; 2. ELONGATION REACTIONS OF LONG-CHAIN FATTY ACIDS; 3. DESATURATION OF LONG-CHAIN FATTY ACID IN MAMMALS; 4. TRANSCRIPTIONAL REGULATION OF DESATURASES AND ELONGASES; 5. SUMMARY AND FUTURE DIRECTIONS; REFERENCES; Chapter 7
  • Phospholipid Synthesis in Mammalian Cells; 1. INTRODUCTION; 2. BIOSYNTHESIS OF PHOSPHATIDIC ACID AND DIACYLGLYCEROL.
  • 3. PHOSPHATIDYLCHOLINE BIOSYNTHESIS AND REGULATION4. PHOSPHATIDYLETHANOLAMINE BIOSYNTHESIS AND REGULATION; 5. PHOSPHATIDYLSERINE BIOSYNTHESIS AND REGULATION; 6. PHOSPHATIDYLINOSITOL AND POLYPHOSPHORYLATED PHOSPHATIDYLINOSITOL; 7. BIOSYNTHESIS OF PHOSPHATIDYLGLYCEROL AND CARDIOLIPIN; 8. FATTY ACID REMODELLING OF PHOSPHOLIPIDS; 9. FUTURE DIRECTIONS; REFERENCES; Chapter 8
  • Phospholipid Catabolism; 1. INTRODUCTION; 2. THE PHOSPHOLIPASE A FAMILY; 3. PHOSPHOLIPASE C; 4. PHOSPHOLIPASE D; 5. FUTURE DIRECTIONS; REFERENCES.
  • Chapter 9
  • The Eicosanoids: Cyclooxygenase, Lipoxygenase and Epoxygenase Pathways.
  • Contents note continued: 4.1. Catabolism of Chylomicrons by Low Desity Lipoprotein Receptor-Related Protein 1
  • 4.2. The So-Called Very Low-Density Lipoprotein Receptor: A Role in Catabolism of Very Low Density Lipoprotein-- 4.3. A Multifunctional Very Low Density Lipoprotein Receptor in the Chicken
  • 5. Other Relatives of the Low-Density Lipoprotein Receptor Family
  • 5.1. ApoER2---A Close Relative of the Very Low Density Lipoprotein Receptor
  • 5.2. Small and Midsize Low-Density Lipoprotein Receptor Relatives: LRP 3, 4, 5 and 6
  • 5.3. The Unusual One: LR11
  • 5.4. Large Low-Density Lipoprotein Receptor Relatives: LRP2 and LRP1B
  • 6. Roles of Lipoprotein Receptors in Signal Transduction
  • 6.1. Genetic Models Reveal New Roles for apoER2 and Very Low Density Lipoprotein Receptor in Signal Transduction
  • 6.2. Signalling through LRP1
  • 7. Scavenger Receptors: Lipid Uptake and Beyond
  • 7.1. Class A Scavenger Receptors
  • 7.2. Lectin-Like Oxidised Low-Density Lipoprotein Receptor
  • 7.3. Class B Scavenger Receptors
  • 8. Outlook
  • References
  • 18. Atherosclerosis / Hong Lu
  • 1. Atherosclerosis
  • 2. Lipoprotein Transport in Atherosclerosis
  • 2.1. Low-Density Lipoprotein
  • 2.2. Very-Low-Density Lipoprotein
  • 2.3. Remnants of VLDL and Chylomicrons
  • 2.4. Lipoprotein(a)
  • 2.5. High-Density Lipoprotein
  • 3. Lipoprotein Receptors and Lipid Transporters
  • 3.1. LDL Receptors
  • 3.2. Scavenger Receptors
  • 3.3. Low-Density Lipoprotein Receptor-Related Protein
  • 3.4. ATP-Binding Cassette Subfamily (ABCs)
  • 4. Contributions of Lipoprotein-Mediated Inflammation to Atherosclerosis
  • 4.1. Cell Types Involved in Atherosclerotic Lesions
  • 4.2. Foam Cells
  • 4.3. Macrophage Polarisation
  • 4.4. Inflammatory Responses
  • 4.5. Atherosclerotic Lesion Macrophage Retention and Emigration
  • 4.6. Atherosclerotic Lesion Regression
  • 5. New Emerging Mechanisms of Lipid Metabolism Influencing Atherosclerosis
  • 5.1. MicroRNAs
  • 5.2. Inflammasomes
  • 5.3. Trimethylamine and Trimethylamine-N-oxide
  • 6. Traditional and Evolving Lipid-Lowering Therapies for the Treatment of Atherosclerosis
  • 6.1. Statins
  • 6.2. Fibrates
  • 6.3. Niacin
  • 6.4. Cholesterol Absorption Inhibitors
  • 6.5. ω-3 Polyunsaturated Fatty Acids
  • 6.6. Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors
  • 6.7. ASO Therapies
  • 6.8. Microsomal Triacylglyceride Transfer Protein Inhibitors
  • 6.9. ACAT and DGAT Inhibitors
  • 6.1. 0 High-Density Lipoprotein Modulating Drugs
  • 7. Future Directions
  • References
  • 19. Diabetic Dyslipidaemia / Gary F. Lewis
  • 1. Introduction to the Typical Dyslipidaemia of Insulin-Resistant States
  • 1.1. Major Dyslipidaemia of Insulin-Resistant States: Hypertriglyceridaemia, Low HDL and Qualitative Changes in Low-Density Lipoprotein (Small, Dense Low-Density Lipoprotein)
  • 1.2. Lipid Profile of Individuals with T1D
  • 1.3. Role of Diabetic Dyslipidaemia in Atherosclerosis and CVD
  • 1.4. Aetiology of the Dyslipidaemia: Genetic and Environmental Factors
  • 2. Dyslipidaemia of Insulin-Resistant States: Key Factors and Mechanisms, with a Focus on Hepatic Lipoprotein Overproduction
  • 2.1. Apolipoprotein B-Containing Lipoproteins: Alterations in Insulin Resistance and T2D
  • 2.2. Molecular Mechanisms Underlying Hepatic Insulin Resistance and Increased VLDL Secretion
  • 2.3. Mechanisms of Hepatic VLDL Overproduction in Insulin Resistance: Multiorgan Cross Talk, Hormones and Dietary Factors
  • 2.4. Association of Fatty Liver/Inflammation and Diabetic Dyslipidaemia
  • 3. Postprandial Dyslipidaemia and Intestinal Chylomicrons Hypersecretion in Insulin-Resistant States
  • 3.1. Mechanisms of Intestinal Lipoprotein Overproduction in Insulin-Resistant States
  • 3.2. Lipid and Carbohydrate Regulation of Intestinal Lipoprotein Secretion
  • 3.3. Alterations in Other Pathways Involved in Lipoprotein Assembly and Secretion
  • 3.4. Gut Peptides and Inflammatory Factors Affect Intestinal Lipoprotein Secretion
  • 4. Low High-Density Lipoprotein in Insulin Resistance and Type 2 Diabetes
  • 4.1. HDL Lowering Due to Increased Catabolism in Hypertriglyceridaemia and Insulin Resistance
  • 4.2. Increased Apolipoprotein A-l Catabolism Due to TG Enrichment, Combined with Increased HL Activity
  • 4.3. Role of Inflammation and Endothelial Lipase in HDL Metabolism
  • 5. Treatment of the Dyslipidaemia of Insulin-Resistant States
  • 5.1. Lifestyle Modification
  • 5.2. Pharmacotherapies
  • 6. Conclusions
  • References.

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