Metabolic syndrome pathophysiology : the role of essential fatty acids

著者

    • Das, Undurti N.

書誌事項

Metabolic syndrome pathophysiology : the role of essential fatty acids

Undurti N. Das

Wiley-Blackwell, 2010

  • : hbk.

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注記

Includes bibliographical references and index

内容説明・目次

内容説明

Metabolic Syndrome Pathophysiology: The Role of Essential Fatty Acids provides current research exploring the links among insulin, insulin receptors, polyunsaturated fatty acids, brain growth and disease. Specific interactions of essential fatty acids and polyunsaturated fatty acids in brain development and several disease groups are described. The role of inflammation in disease and how fatty acids regulate low-systemic inflammation are examined and explained. Metabolic and neurologic dynamics are presented to provide a linkage between the presence of omega-3 and omega-6 and protection against diseases and conditions such as diabetes mellitus, obesity, autoimmune diseases and hypertension.

目次

Preface xiii 1 Introduction 1 2 History, Definition, and Diagnosis of the Metabolic Syndrome 4 Historical Aspects of the Metabolic Syndrome 4 Definition and Diagnosis of the Metabolic Syndrome Suggested by Various Groups and Associations 5 3 Insulin Resistance in the Metabolic Syndrome 13 Is Insulin Resistance Responsible for the Metabolic Syndrome? 13 Exercise and Insulin Resistance 14 Anti-inflammatory Nature of Exercise 15 4 Is It Necessary to Redefine the Metabolic Syndrome? 22 Criteria 23 5 Is Insulin Resistance a Disorder of the Brain? 26 Parasympathetic and Sympathetic Tones and Insulin Resistance 26 Hypothalamo-pituitary-adrenal Pathway and Parasympathetic and Sympathetic System, and GLUT-4 and Hypothalamic Neuropeptide Y in Insulin Resistance, Obesity, and the Metabolic Syndrome 27 Interaction(s) among NPY, Leptin, GLUT-4, Melanocortin, and Insulin and Its Relevance to Obesity, Insulin Resistance, and the Metabolic Syndrome 29 Insulin and Brain 31 Insulin and Brain Monoamines 34 Obesity and Basal Energy Expenditure 39 6 Obesity 43 Definition of Obesity 44 Incidence and Prevalence of Obesity 44 Obesity Could Run in the Family 45 Growth of Fast Food Industry and Obesity 45 Why Is Obesity Harmful? 46 Genetics of Obesity 47 Gene Expression Profile in Obesity 49 Biochemical and Functional Differences between Adipose Cells of Different Regions 49 Intramyocellular Lipid Content and Insulin Resistance 51 Intramyocellular Lipid Droplets and Insulin Resistance 53 Intramyocellular Lipid Droplets, Insulin Resistance, Perilipins, and HSL 54 Perilipins in Humans 55 Factors Regulating the Expression and Action of Perilipin 56 Perilipins and Inflammation 59 Low-grade Systemic Inflammation Occurs in Obesity 59 What Causes Abdominal Obesity? 61 11 -Hydroxysteroid Dehydrogenase Type 1 (11 -HSD-1) Enzyme and Obesity 61 Glucocorticoids and Perilipins 63 Glucocorticoids, TNF- , and Inflammation 64 Perilipins, 11 -HSD-1, and Abdominal Obesity and the Metabolic Syndrome in High-Risk Groups Such as South Asians 65 7 Perinatal Nutrition and Obesity 74 Appetite Regulatory Centers Develop during the Perinatal Period 74 Ventromedial Hypothalamus Plays a Significant Role in the Development of Obesity, Type 2 Diabetes Mellitus, and the Metabolic Syndrome 76 Glucokinase in Hypothalamic Neurons and VMH Lesion in Goto-Kakizaki Rats and Their Relationship to Obesity, Type 2 Diabetes Mellitus, and the Metabolic Syndrome 77 Insulin and Insulin Receptors in the Brain and Their Role in the Pathobiology of Obesity, Type 2 Diabetes Mellitus, and the Metabolic Syndrome 78 NPY, Insulin, and Nitric Oxide in Obesity, Type 2 Diabetes Mellitus, and the Metabolic Syndrome 80 Insulin, Endothelial Nitric Oxide, and Metabolic Syndrome 81 Perinatal Programming of Adult Diseases 81 Fetal Nutrition Influences the Developing Neuroendocrine Hypothalamus 82 8 Essential Hypertension 86 Prevalence and Incidence of Hypertension 86 Free Radicals in the Pathobiology of Hypertension 88 Increase in Superoxide Anion Production in Hypertension: How and Why? 89 Mechanism(s) of Induction of Hypertension by Superoxide Anion 91 Role of NO in Hypertension 92 Salt, Cyclosporine, and Calcium Modulate O2 . and Endothelial NO Generation 94 L-Arginine, NO, and Asymmetrical Dimethylarginine in Hypertension and Pre-eclampsia 95 Antihypertensive Drugs Suppress Superoxide Anion and Enhance NO Generation 97 Transforming Growth Factor- , NO, and Hypertension 97 9 Dietary Factors and Hypertension 105 Carbohydrate-rich and High-fat Diet and Hypertension 105 Fructose-induced Hypertension and Insulin Resistance and Its Modulation by Dietary Salt 106 Energy-dense Diet, Salt, and Hypertension 106 Diet-induced Hypertension, Renin-Angiotensin-Aldosterone System, and Nitric Oxide 107 High-sugar and High-fat-induced Hypertension and Reactive Oxygen Species and Nitric Oxide 108 High-fructose and Salt-induced Hypertension and Insulin Resistance 109 High-fat and High-carbohydrate-induced Hypertension and Sympathetic Nervous Activity 111 10 Is Hypertension a Disorder of the Brain? 113 NO Synthase (NOS) Activity in the Brain, Kidney, and Endothelium and Its Relationship to Hypertension 114 Reduced Hypothalamic NOS Produces Hypertension without Altering Hypothalamic Blood Flow 115 Hypothalamic NO Regulates Sympathetic Outflow 116 Steroid-induced Hypertension and Hypothalamus 117 Exercise Enhances Hypothalamic NOS Activity 119 Both Hypertension and Type 2 Diabetes Mellitus and Hence the Metabolic Syndrome Are Disorders of the Brain 119 11 Type 2 Diabetes Mellitus 122 Type 1 Diabetes Mellitus 122 Pathobiology of Type 1 Diabetes 123 Type 2 Diabetes Mellitus 125 Diagnostic Criteria for DM 126 Impaired Glucose Tolerance and Impaired Fasting Glucose 127 Definition of Gestational Diabetes Mellitus 127 Diagnostic Criteria for GDM 127 12 Pathophysiology of Type 2 Diabetes Mellitus with Particular Reference to Hypothalamus 130 Type 2 Diabetes Mellitus as a Disorder of the Brain 130 Liver Communicates with the Brain through the Vagus 131 Liver and Pancreatic Cells Communicate with Each Other through the Vagus 132 The Gut-brain-liver Axis Is Activated by Long-chain Fatty Acids (LCFAs or LCPUFAs) 132 BDNF and Obesity 136 BDNF and Type 2 Diabetes Mellitus in Humans 137 Insulin, Melanocortin, and BDNF 138 Ghrelin, Leptin, and BDNF 138 Low-grade Systemic Inflammation Occurs in Obesity and Type 2 Diabetes Mellitus 140 BDNF and Inflammation 141 13 Insulin and Insulin Receptors in the Brain and Their Role in the Pathogenesis of Obesity and Type 2 Diabetes Mellitus 146 Insulin and Insulin Receptors in the Brain 146 Glucose Transporters and Glucokinase in Hypothalamus 147 Neuron-specific Disruption of the Insulin Receptor Gene (NIRKO) 147 Insulin and Hypothalamic Neuropeptides 148 Leptin Receptors on Pancreatic Cells 148 Glucagon-like Peptide, Insulin, and the Metabolic Syndrome 149 14 Insulin, Endothelial Nitric Oxide, and the Metabolic Syndrome 156 Insulin Resistance and Nitric Oxide 156 Ghrelin Improves Endothelial Function in the Metabolic Syndrome 159 Cross-talk between Insulin and Renin-Angiotensin-Aldosterone System 159 Pro-inflammatory Cytokines Produce Insulin Resistance 161 15 Obesity, Type 2 Diabetes Mellitus, the Metabolic Syndrome, and the Gut Microbiota 167 Gut Flora, Diet, Obesity, and Inflammation 167 Germ-free Mice Are Resistant to Obesity 168 Enteroendocrine Cell Expression of Gpr41 and Obesity 169 Low-grade Systemic Inflammation, Diet, and Obesity 171 Gastric Bypass Surgery for Obesity and the Metabolic Syndrome 171 Diet, Gut, Liver, Adipose Tissue, and Hypothalamus in Obesity and the Metabolic Syndrome 173 16 Is It Possible That the Metabolic Syndrome Originates in the Perinatal Period? 177 Perinatal Programming of Appetite Regulatory Centers and Hypothalamic Centers 177 Insulin and Insulin Receptors in the Brain 178 17 Essential Fatty Acids: Biochemistry and Physiology 181 Metabolism of EFAs 181 Dietary Sources of EFAs 183 Modulators of Metabolism of EFAs 183 PUFAs and SREBPs 184 Cholesterol, Saturated Fats, and Trans-fats Interfere with the Activity of 6 and 5 Desaturases 185 Actions of EFAs and Their Metabolites 188 Brief Description of Formation of Lipoxins, Resolvins, Neuroprotectin D1 (Protectins), and Maresins 193 Nitrolipids 194 18 Role of EFAs/PUFAs in Brain Growth and Development and Pathophysiology of the Metabolic Syndrome 201 PUFAs in Brain Growth and Development 201 RAR-RXR Nuclear Receptors, PUFAs, and Neuronal Growth 202 Interaction among TNF- , AA/EPA/DHA, and Insulin and Their Role in Neuronal Growth and Synapse Formation 202 PUFAs and Catenin, wnt, and Hedgehog Signaling Pathway in Brain Growth and Development 203 -Catenin-Wnt Signaling and PUFAs 205 Modulation of the Secretion and Function of NMDA, -Aminobutyric Acid (GABA), Serotonin, and Dopamine by PUFAs 205 Leptin Regulates NPY/AgRP and POMC/CART Neurons and Programs Hypothalamic "Body Weight/Appetite/Satiety Set Point" 209 PUFAs Regulate Leptin, NPY/AgRP, and POMC/CART Neurons and Participate in Programming Hypothalamic "Body Weight/ Appetite/Satiety Set Point" 212 PUFAs, Insulin, and Acetylcholine Not Only Interact among Themselves but Are Also Neuroprotective in Nature 215 PUFAs and Insulin Resistance 215 Maternal Diet Influences 6 and 5 Desaturases and Leptin Levels 216 Interaction(s) among Hypothalamic Neuropeptides, Gut, Adipose Tissue, Insulin, Cytokines, and Free Radicals and Its Relevance to the Pathophysiology of the Metabolic Syndrome 217 Hypothalamic Gene Expression Profile in the RYGB Animal Model 218 Increased Phospholipase A2 Expression after RYGB Surgery and Its Relevance to Suppression of Low-grade Systemic Inflammation in the Obese and Formation of Anti-inflammatory Lipids 219 Expression of Gene for eNOS in RYGB 220 RYGB-induced Weight Loss Is Due to Changes in the Levels of Hypothalamic Neuropeptides and Monoamines 220 What Are the Diagnostic and Prognostic Implications of This Knowledge? 221 Therapeutic Implications 223 PUFAs and Endocannabinoids 224 PUFAs and Type 2 Diabetes Mellitus 224 Hypothalamic PUFAs Regulate Insulin Secretion and Glucose Homeostasis by Influencing ATP-sensitive K+ Channels 225 Vagus as the Communicator between Gut, Liver, and Hypothalamus 227 19 EFAs/PUFAs and Their Metabolites in Insulin Resistance 240 GLUT-4 in Insulin Resistance 240 Tumor Necrosis Factor Induces Insulin Resistance 242 Caloric Restriction Influences Insulin Signaling Pathway, Antioxidants, daf genes, PTEN, Sirtuins (Silent Mating Type Information Regulation 2 Homologue), and Longevity and Their Relationship to Insulin Resistance 242 PUFAs Can Reduce Insulin Resistance 244 PUFAs, GLUT-4, TNF- , Anti-oxidants, daf Genes, SIRT1, and PPARs 245 Clinical Implications of the Interactions among PUFAs, daf Genes, PPARs, and Sirtuins 246 20 EFAs/PUFAs and Atherosclerosis 252 Atherosclerosis Is a Systemic Inflammatory Condition 252 Cross-talk among Platelets, Leukocytes, and Endothelial Cells 253 Leukocytes and Atherosclerosis 254 EFAs Modulate Uncoupling Protein-1 Expression 255 Interaction(s) among -3 and -6 Fatty Acids and Trans-fats and Saturated Fats 255 Atheroprotective Actions of -3 and -6 Fatty Acids: How and Why? 259 Index 265

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