Biochemistry of Lipids Lipoproteins and Membranes 7th Edition by Neale Ridgway, Roger McLeod ISBN 0128240482 978-0128240489

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ISBN 10: 0128240482
ISBN 13: 978-0128240489
Author: Neale Ridgway, Roger McLeod 

Biochemistry of Lipids, Lipoproteins and Membranes, Seventh Edition serves as a comprehensive, general reference book for scientists and students studying lipids, lipoproteins and membranes. Here, across 19 chapters, leaders in the field summarize fundamental concepts, recent research developments, data analysis, and implications for human disease and intervention. Topics discussed include lipid biology in both prokaryotes and eukaryotes, fatty acid synthesis, desaturation and elongation, and pathways leading to synthesis of complex phospholipids, sphingolipids and their structural variants. Chapters also examine how bioactive lipids are involved in cell signaling, with an emphasis on disease implications and pathological consequences.

As the field advances, each chapter in this new edition has been fully revised to address emerging topics, with all-new coverage of lipid droplets and their role as regulatory organelles for energy homeostasis, as well as their relationship to obesity, liver disease and diabetes. Evolving research in fatty acid handling and storage in eukaryotes is also discussed in-depth, with new sections addressing fatty acid uptake, activation and lipolysis.

• Fully revised to cover new and emerging topics
• Provides an important bridge between broad-based biochemistry research and application
• Presents key concepts that are supported by figures and models to improve understanding
• Includes references from current literature in each chapter to facilitate in-depth study

Biochemistry of Lipids, Lipoproteins and Membranes 7th Table of contents:

Chapter 1 Functional roles of lipids in biological membranes

List of abbreviations

1: Introduction and overview

2: Diversity in lipid structure

2.1: Glycerolipids

2.2: Saccharolipids

2.3: Sphingolipids

3: Properties of lipids in solution

3.1: Why do membranes form?

3.2: Physical properties of membrane bilayers

3.3: What does the membrane bilayer look like?

4: Engineering of membrane lipid composition

4.1: Alteration of lipid composition in bacteria

5: Role of lipids in cell function

5.1: The bilayer as a supramolecular lipid matrix

5.2: MP structure and function: lipids in charge?

5.3: Do lipids tell proteins how to fold and insert?

5.4: Heterologous organisation of membrane components

5.5: Lipids and conformational diseases

6: Is the fluid mosaic membrane model still relevant?

7: General conclusions on lipid function

8: Future directions

Chapter 2 Methods of lipid analysis

List of abbreviations

1: Introduction to lipidomics

1.1: Lipid diversity

2: Sample collection/sampling

2.1: Sample collection

2.2: Lipid extraction from biological samples

2.3: Solid-phase extraction for sample enrichment

2.4: Derivatisation approaches for lipid analysis

3: Direct infusion and chromatography-based approaches for lipid analysis

3.1: Thin-layer chromatography

3.2: Gas chromatography

3.3: High-performance and ultra-high-pressure liquid chromatography

3.4: Supercritical fluid chromatography

4: Quantitation of lipid levels

4.1: Quality control checks

5: Mass spectrometry for lipid analysis

5.1: Ionisation sources

5.2: Mass analysers

5.3: Fragmentation techniques used in lipid analysis

5.4: Ion mobility

5.5: Mass spectrometry imaging

6: LC-MS data processing and future directions

Chapter 3 Fatty acid and phospholipid biosynthesis in prokaryotes

List of abbreviations

1: Overview of bacterial lipid metabolism

2: Membrane systems of bacteria

3: The initiation module

3.1: Acyl carrier protein

3.2: Acetyl-coenzyme A carboxylase

3.3: Malonyl transacylase

3.4: 3-ketoacyl-acyl carrier protein synthase III

3.5: Regulation in the initiation module

4: The elongation module

4.1: 3-ketoacyl-acyl carrier protein synthases I and II

4.2: 3-ketoacyl-acyl carrier protein reductase

4.3: 3-hydroxyacyl-acyl carrier protein dehydratases

4.4: Enoyl-acyl carrier protein reductase

4.5: Regulation in the elongation module

4.6: Bacteria with type I fatty acid synthase

5: The acyltransfer module

5.1: The PlsB/PlsC system

5.2: The PlsX/PlsY/PlsC system

5.3: Regulation in the acyltransfer module

5.4: Use of extracellular fatty acids

5.5: Thioesterases

5.6: Fatty acids as a carbon source

6: The phospholipid module

6.1: Phosphatidate cytidylyltransferase

6.2: Phosphatidylethanolamine production

6.3: Phosphatidylserine decarboxylase

6.4: Phosphatidylglycerol synthesis

6.5: Cardiolipin biosynthesis

6.6: Use of phospholipid headgroups

6.7: Modification of phospholipids

6.8: Phospholipid diversity in bacteria

6.9: Membrane lipids lacking phosphorus

6.10: Regulation in the phospholipid module

7: Genetic regulation of lipid metabolism

7.1: Gram-negative bacteria

7.2: Gram-positive bacteria

7.3: Stress response regulators

8: Future directions

Chapter 4 Lipid metabolism in plants

List of abbreviations

1: Introduction

2: Plant lipid geography

2.1: Plastids

2.2: Endoplasmic reticulum and lipid bodies

2.3: Mitochondria

2.4: Peroxisomes and glyoxysomes

3: Acyl-acyl carrier protein synthesis in plants

3.1: Components of plant fatty acid synthase

3.2: The first double bond is introduced by soluble acyl-acyl carrier protein desaturases

3.3: Acyl-acyl carrier protein thioesterases release fatty acids for export

4: Acetyl-coenzyme A carboxylase and control of fatty acid synthesis

4.1: Most plants have two acetyl-coenzyme A carboxylases

4.2: Acetyl-coenzyme A carboxylase is a control point for fatty acid synthesis

5: Phosphatidic acid synthesis occurs via prokaryotic and eukaryotic acyltransferases

5.1: Plastidial acyltransferases use acyl-acyl carrier protein substrates

5.2: Extraplastidial acyltransferases use acyl-coenzyme A substrates

5.3: The 16:3 and 18:3 plants have different proportions of prokaryotic flux

6: Membrane glycerolipid synthesis

6.1: Lipid trafficking between plastids and endomembranes

6.2: Glycerolipids are substrates for polyunsaturated fatty acid synthesis

6.3: Some plants use endoplasmic reticulum glycerolipids as substrates for production of unusual fatty acids

7: Lipid storage in plants

7.1: Lipid body structure and biogenesis

7.2: The pathways of triacylglycerol biosynthesis

7.3: Control of triacylglycerol yield

7.4: Control of triacylglycerol composition

7.5: Triacylglycerols in vegetative tissues

7.6: Triacylglycerol engineering: some case studies

8: Protective lipids: cutin, waxes, suberin and sporopollenin

8.1: Fatty acid elongation and wax production

9: Sphingolipid biosynthesis

10: Oxylipins as plant hormones

11: Sterol and isoprenoid biosynthesis

12: Future prospects

Chapter 5 Fatty acid handling in mammalian cells

List of abbreviations

1: Introduction

2: Fatty acid biosynthesis

2.1: Acyl-CoA carboxylase

2.2: Cytosolic fatty acid synthase

2.3: Mitochondrial fatty acid synthase

3: Fatty acid uptake, activation and trafficking

3.1: CD36

3.2: Fatty acid transport proteins/acyl-CoA synthetase very long chain

3.3: Acyl-CoA synthetases

3.4: Fatty acid-binding proteins

3.5: Acyl-CoA-binding protein

4: Fatty acid esterification into TG

4.1: Monoacylglycerol acyltransferases

4.2: Diacylglycerol acyltransferases

5: Fatty acid utilisation for energy

5.1: Lipolysis of stored triacylglycerol

5.2: Fatty acid oxidation

5.3: Fatty acids and thermogenesis

6: Fatty acids and signalling

6.1: Fatty acids as ligands for nuclear receptors

6.2: Free fatty acid receptors

6.3: Fatty acids as signalling molecules

7: Fatty acids and disease pathogenesis

7.1: Insulin resistance

7.2: Endoplasmic reticulum stress

7.3: Inflammation

8: Future directions

Chapter 6 Fatty acid desaturation and elongation in mammals

List of abbreviations

1: Introduction

1.1: Nomenclature and sources of long-chain fatty acids

2: Elongation reactions of long-chain fatty acids

2.1: Microsomal fatty acid elongation

2.2: β-Hydroxyacyl-CoA dehydratase

2.3: Mitochondrial fatty acid elongation

2.4: Peroxisomal fatty acid elongation

3: Desaturation of long-chain fatty acid in mammals

3.1: Δ9 desaturase

3.2: Δ5 and Δ6 desaturases

3.3: Fatty acid desaturase 3

4: Functions of fatty acids synthesised by Δ9, Δ6 and Δ5 desaturase

4.1: Monounsaturated fatty acids (n-9)

4.2: Polyunsaturated fatty acids (n-3 and n-6)

5: Transcriptional regulation of desaturases and elongases

5.1: Sterol regulatory element-binding proteins

5.2: Liver X receptors

5.3: Peroxisome proliferator-activated receptors

5.4: Carbohydrate response element-binding protein

6: Summary and future directions

Chapter 7 Phospholipid synthesis in mammalian cells

List of abbreviations

1: Introduction

2: Biosynthesis of phosphatidic acid and diacylglycerol

2.1: Glycerol-3-phosphate acyltransferases

2.2: 1-Acylglycerol-3-phosphate acyltransferases

2.3: Phosphatidic acid phosphatases

2.4: DAG kinases

3: Synthesis of ether and plasmalogen lipids

4: Phosphatidylcholine biosynthesis and regulation

4.1: PC synthesis by the CDP-choline/Kennedy pathway

4.2: Choline transporters

4.3: Choline kinase

4.4: CTP: phosphocholine cytidylyltransferase

4.5: Post-transcriptional regulation of CCT

4.6: Choline phosphotransferase

4.7: Phosphatidylethanolamine N-methyltransferase

5: Phosphatidylethanolamine biosynthesis and regulation

5.1: Functions of PE

5.2: The CDP-ethanolamine pathway

5.3: The phosphatidylserine decarboxylase pathway for PE synthesis

6: Phosphatidylserine biosynthesis and regulation

6.1: Functions of PS

6.2: Serine base exchange pathways: phosphatidylserine synthases 1 and 2

7: Biosynthesis of CDP-diacylglycerol

8: Biosynthesis of phosphatidylglycerol and cardiolipin

8.1: Structure and function of phosphatidylglycerol and cardiolipin

8.2: PG and cardiolipin biosynthetic pathways

9: Phosphatidylinositol and polyphosphorylated PI

9.1: Cellular functions of PI and its phosphorylated derivatives

9.2: Functions of phosphatidylinositol polyphosphates

9.3: Phosphatidylinositol kinases and phosphatases

10: Fatty acid remodelling of phospholipids

11: Future directions

Chapter 8 Phospholipid catabolism

List of abbreviations

1: Introduction

2: Phospholipase A1

3: Phospholipase A2

3.1: Secretory phospholipase A2

3.2: Cytosolic phospholipase A2 (group IV PLA2)

3.3: Calcium-independent PLA2 (group VI iPLA2)

3.4: Platelet-activating factor acetylhydrolases (group VII/VIII or PAF-AHs)

3.5: Lysosomal PLA2 (group XV PLA2)

3.6: Adipocyte-specific PLA2 (group XVI or AdPLA)

4: Phospholipase B

5: Phospholipase C

6: Phospholipase D

7: Measuring the activity of phospholipases

7.1: Radioactive assays

7.2: Fluorescent and colourimetric assays

7.3: Measurement of substrates or catalytic products using genetically encoded biosensors

7.4: Mass spectrometry

8: Concluding remarks

Chapter 9 Sphingolipids

List of abbreviations

1: Introduction

2: Nomenclature and structure

3: SL biosynthesis

3.1: SPT and 3-ketosphinganine reductase

3.2: Ceramide synthases, dihydroceramide desaturase and O-acyl-ceramide synthase

3.3: Ceramide transport between the ER and the Golgi apparatus

3.4: Formation of sphingosine 1-phosphate

3.5: GSL synthesis and transport

4: Sphingolipid degradation

5: Sphingolipid signalling and roles in cell regulation

6: Sphingolipid biophysics

7: SLs in disease pathology

7.1: Serine palmitoyl transferase

7.2: Ceramide synthases

7.3: Dihydroceramide desaturase

7.4: GSL synthesis

7.5: GSL degradation

7.6: ASM and ceramidases

7.7: S1P, S1PRs, sphingosine kinase and sphingosine phosphate lyase

8: Perspectives

Chapter 10 Cholesterol synthesis

List of abbreviations

1: Introduction

1.1: What is cholesterol?

1.2: The cholesterol synthesis pathway

1.3: The functions of cholesterol

1.4: Cholesterol in the body

1.5: Where is cholesterol made within cells?

1.6: Cholesterol homoeostasis

2: Cholesterol synthesis – a historical overview

3: Targeting cholesterol synthesis therapeutically

3.1: How statins work to decrease blood cholesterol levels

4: Sterol pathway intermediates

4.1: Overview

4.2: Functions of the intermediates

4.3: Diseases resulting from defective cholesterol synthesis

5: Enzymes of cholesterol biosynthesis

5.1: Acetyl-CoA to mevalonic acid (Figure 10.7)

5.2: Mevalonic acid to squalene (Figure 10.8)

5.3: Squalene cyclisation to lanosterol (Figure 10.9)

5.4: Lanosterol metabolism in the Bloch and Kandutsch–Russell pathways (Figure 10.10)

5.5: Lanosterol conversion to penultimate intermediates (Figure 10.11)

5.6: Terminal enzymes in cholesterol synthesis (Figure 10.12)

6: Oxysterols

7: Regulation of cholesterol synthesis

7.1: Transcription

7.2: Post-translational regulation

7.3: Regulation by non-coding RNAs

8: Summary

Chapter 11 Structure and function of lipid droplets

List of abbreviations

1: Introduction

2: The structure of LDs

2.1: The monolayer of LD surface lipids

2.2: Lipid droplet proteome

3: The biogenesis and growth of LDs

3.1: The synthesis of core neutral lipids in the ER

3.2: TAG nucleation and LD emergence from the ER

3.3: Budding/emergence of nascent lipid droplets from the ER

3.4: LD growth and separation from the ER

3.5: LD growth by fusion

3.6: Seipin in LD biogenesis and growth

3.7: The biogenesis of ER luminal LDs

3.8: The biogenesis of nucleoplasmic LDs

4: LD contacts with organelles

4.1: ER-LD contacts and bridges

4.2: Mitochondrial LD contacts

4.3: Other organelle LD contacts

5: Lipolysis of neutral lipids

5.1: ATGL/PNPLA2

5.2: Hormone-sensitive lipase

5.3: Monoacylglycerol lipase

5.4: Patatin-like phospholipase domain-containing protein 3

5.5: Carboxylesterase 3/triacylglycerol hydrolase

5.6: Hormonal regulation of neutral lipolysis

6: Acid lipolysis and lipophagy

6.1: Lysosomal acid lipase

6.2: Lipophagy

7: LDs and cellular stress

8: LDs in infection and immunity

9: Future directions

Chapter 12 Bile acid metabolism

List of abbreviations

1: Introduction

2: Bile acid structure and physical properties

3: Biosynthesis of bile acids

3.1: Biosynthetic pathway

3.2: Inherited defects in bile acid synthesis

3.3: Regulation of bile acid biosynthesis

3.4: Secondary metabolism of bile acids

4: Enterohepatic circulation of bile acids

4.1: Hepatic bile acid transport

4.2: Intestinal absorption of bile acids

5: Bile acids as signalling molecules

6: Future directions

Chapter 13 Lipid modification of proteins

List of abbreviations

1: Introduction

2: Attachment of fatty acids to proteins

2.1: N-myristoylation

2.2: S-palmitoylation

2.3: N-palmitoylation

2.4: Acylation with other fatty acids

3: Attachment of cholesterol to hedgehog proteins

4: Attachment of isoprenoids to proteins

4.1: Farnesylation

4.2: Geranylgeranylation

5: Attachment of phospholipids and diacylglycerol lipids to proteins

5.1: GPI anchors

5.2: PE attachment to the Atg8 and LC3 autophagy proteins

5.3: Bacterial lipoproteins

6: Spotlight on inhibitors of lipid-modifying enzymes and their roles in disease

6.1: Inhibitors of NMT

6.2: Inhibitors of S-palmitoylation and depalmitoylation

6.3: Inhibitors of N-palmitoylation and palmitoleoylation

6.4: FTase and GGTase I inhibitors

6.5: Defects in GPI anchor biosynthesis

7: Future directions and challenges

Chapter 14 Inter- and intra-membrane lipid transport

List of abbreviations

1: Introduction

2: The modes of intracellular lipid transport

2.1: Vesicular transport of lipids

2.2: Non-vesicular lipid transport

2.3: Spontaneous diffusion of lipids

2.4: Lipid transfer proteins

2.5: Membrane contact sites

2.6: Co-operation of lipid transport via vesicles and LTPs

3: Local synthesis of lipids by organelle-associated enzymes and inter-organelle transport of their substrates

3.1: Organelle-specific synthesis of sphingomyelin and glycosphingolipids

3.2: The synthesis of PE in mitochondria

3.3: Synthesis and catabolism of PI4P and PI(4,5)P2

3.4: Synthesis of neutral lipids in the ER and their deposition into lipid droplets

4: Trans-bilayer lipid asymmetry and intra-membrane transport

4.1: Flippases

4.2: Floppases

4.3: Scramblases

5: Conclusions and future perspectives

Chapter 15 High-density lipoproteins

List of abbreviations

1: Introduction

2: High-density lipoprotein formation

2.1: HDL composition and subclasses

2.2: HDL apolipoproteins

2.3: ABCA1 and initial formation of HDLs

2.4: Additional mechanisms of cholesterol efflux to HDLs

3: High-density lipoprotein remodelling and lipid transfer

3.1: Lecithin cholesterol acyltransferase

3.2: Cholesteryl ester transfer protein

3.3: Phospholipid transfer protein

3.4: Hepatic lipase

3.5: Endothelial lipase

3.6: Scavenger receptor class B, type 1

4: Extremes of high-density lipoprotein cholesterol levels and relationship to atherosclerosis

4.1: ApoAI deficiency

4.2: ABCA1 deficiency

4.3: LCAT deficiency

4.4: Cholesteryl ester transfer protein deficiency

4.5: Hepatic lipase and endothelial lipase deficiency

4.6: SR-B1 deficiency

5: Protective actions of high-density lipoproteins

5.1: Anti-inflammatory effects

5.2: Protection of vascular endothelium

5.3: Antioxidant effects

5.4: Antithrombotic effects

5.5: Effects on glucose metabolism

5.6: Other protective actions of HDLs

5.7: Loss of protective actions of HDLs and generation of pro-atherogenic HDL

6: High-density lipoprotein-raising interventions

7: Summary and future directions

Chapter 16 Assembly and secretion of triacylglycerol-rich lipoproteins

List of abbreviations

1: Overview of apolipoprotein B-containing lipoproteins

2: Structure and regulation of the apolipoprotein B gene

3: Structural features of apolipoprotein B

3.1: Computer models

3.2: Experimental evidence

3.3: Homology modelling

3.4: Post-translational modifications

4: Assembly of hepatic very-low-density lipoproteins

4.1: Role of microsomal triacylglycerol transfer protein

4.2: VLDL heterogeneity

4.3: Exchangeable apolipoproteins

5: Regulation of hepatic very-low-density lipoprotein assembly and secretion

5.1: Triacylglycerol supply

5.2: Phospholipid supply

5.3: Cholesterol synthesis

5.4: Cellular trafficking

5.5: Pharmacologic agents that regulate VLDL secretion

6: Intracellular degradation of apolipoprotein B

6.1: Ubiquitin-proteasome system

6.2: Non-proteasomal mechanisms of apoB degradation

7: Dysregulation of very-low-density lipoprotein assembly and secretion

7.1: Insulin resistance

7.2: Non-alcoholic fatty liver disease

8: Assembly and secretion of chylomicrons

8.1: Similarities to VLDL assembly

8.2: Distinguishing features

9: Limitations of current knowledge

10: Future directions

Chapter 17 Lipoprotein(a)

List of abbreviations

1: Introduction

2: Lp(a) and apo(a) structure and evolution

2.1: Structure of Lp(a)

2.2: Structure of apo(a)

2.3: Properties of apo(a) kringles – lysine binding and glycosylation

2.4: Evolution of LPA: the gene encoding apo(a)

3: Biosynthesis of Lp(a)

3.1: Transcriptional regulation of LPA

3.2: Secretion of apo(a) from hepatocytes

3.3: Assembly of Lp(a) particles

4: Removal of Lp(a) from the circulation

5: Genetics of Lp(a)

6: Lp(a) as a risk factor for cardiovascular diseases

6.1: Lp(a) and CHD risk

6.2: Lp(a) and calcific aortic valve disease

7: Challenges in Lp(a) measurement

8: Mechanism of action of Lp(a) in cardiovascular disease

8.1: The role of Lp(a) in fibrinolysis and thrombosis

8.2: Mechanism of Lp(a) action in atherosclerosis and aortic valve disease – a key role for oxidised phospholipids

9: Pharmaceutical approaches to Lp(a) lowering: progress to date

10: Challenges and perspectives in the Lp(a) field

Chapter 18 Lipoprotein receptors

List of abbreviations

1: Introduction

2: LDLR family

2.1: Evolution

2.2: Structural organisation

2.3: General properties and function

2.4: LDLR family and Wnt signalling

2.5: LDLR family and cholesterol metabolism in the brain

3: Low-density lipoprotein receptor

3.1: Gene and protein organisation

3.2: LDLR function in health and disease

3.3: Regulation of LDLR function

4: Very-low-density lipoprotein receptor

4.1: Gene and protein organisation

4.2: VLDLR function in lipid metabolism and in the CNS

4.3: Regulation of VLDLR function

5: APOER2/LRP8

5.1: Gene and protein organisation

5.2: APOER2 function in the developing and adult brain

5.3: APOER2 and cardiovascular diseases

5.4: APOER2 and selenium transport

6: LRP1

6.1: Gene and protein organisation

6.2: LRP1 in lipid metabolism

6.3: LRP1 and vasculature

6.4: LRP1 and glucose metabolism

6.5: LRP1 and inflammation

6.6: LRP1 and other implications

7: LRP1B

7.1: Gene and protein organisation

7.2: LRP1B in health and disease

8: LRP2/megalin

8.1: General properties and structure

8.2: LRP2 function in health and disease

8.3: Regulation of LRP2 function

9: LRP4/MEGF7

9.1: Gene and protein organisation

9.2: LRP4 and Wnt/β-catenin signalling

9.3: LRP4 as a co-receptor during NMJ formation

9.4: LRP4 function in the brain

10: LRP5 and LRP6

10.1: Gene and protein organisation

10.2: LRP5/6 as co-receptors in the Wnt/β-catenin signalling pathway

10.3: Regulation of Lrp5/6 activity

10.4: LRP5/6 function in health and disease

11: SorLA/LR11

11.1: Gene and protein organisation

11.2: General function as sorting and endocytic receptor

11.3: SorLA in health and disease

12: Scavenger receptors

12.1: Definition and classification

12.2: Scavenger receptor class A

12.3: Scavenger receptor class B

12.4: Scavenger receptor class E

13: Conclusion

Competing interests

Funding

Chapter 19 Atherosclerosis

List of abbreviations

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) (Lp(a))

2.5: High-density lipoprotein

3: Lipoprotein receptors and lipid transporters

3.1: LDL receptors

3.2: The LDL receptor family

3.3: Scavenger receptors

3.4: ATP-binding cassette subfamily

4: Contributions of lipoprotein-mediated inflammation to atherosclerosis

4.1: Cell types involved in atherosclerotic lesions

4.2: Foam cells

4.3: Macrophage proliferation

4.4: Macrophage polarisation

4.5: Inflammatory responses

4.6: Atherosclerotic lesion macrophage retention and emigration

4.7: Atherosclerotic lesion regression

4.8: Re-classification of cells in atherosclerotic plaques

5: New emerging mechanisms of lipid metabolism influencing atherosclerosis

5.1: Non-coding RNAs

5.2: Inflammasomes

5.3: Trimethylamine and trimethylamine-N-oxide

6: Traditional and evolving lipid-lowering therapies for the treatment of atherosclerosis

6.1: Treatments for hypercholesterolaemia

6.2: Treatment for lowering Lp(a)

6.3: LDL-C lowering therapies specific for homozygous familial hypercholesterolaemia

6.4: Treatments for hypertriglyceridaemia

6.5: HDL-modulating drugs

7: Future directions

Chapter 20 Diabetic dyslipidaemia

List of abbreviations

1: Introduction to the typical dyslipidaemia of insulin-resistant states

1.1: Major dyslipidaemia of insulin-resistant states: hypertriglyceridaemia, low HDL cholesterol and qualitative changes in LDL particles (small, dense LDL)

1.2: Lipid profile of individuals with type 1 diabetes

1.3: Role of diabetic dyslipidaemia in atherosclerosis and CVD

1.4: Etiology of 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: multi-organ crosstalk, hormones and dietary factors

2.4: Association of fatty liver/inflammation and diabetic dyslipidaemia

3: Postprandial dyslipidaemia and intestinal chylomicron 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 HDL in insulin resistance and T2D

4.1: HDL-lowering due to increased catabolism in hypertriglyceridaemia and insulin resistance

4.2: Increased apoA-I catabolism due to TG enrichment, combined with increased HL activity

4.3: The role of HDL functionality in atherosclerotic CVD

5: Treatment of the dyslipidaemia of insulin-resistant states

5.1: Lifestyle modification

5.2: Pharmacotherapies

6: Conclusions

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