The Role of Essential Fatty Acids
Buch, Englisch, 268 Seiten, Format (B × H): 175 mm x 246 mm, Gewicht: 717 g
ISBN: 978-0-8138-1553-4
Verlag: Wiley
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.
Autoren/Hrsg.
Fachgebiete
- Medizin | Veterinärmedizin Medizin | Public Health | Pharmazie | Zahnmedizin Medizin, Gesundheitswesen Ernährungsmedizin, Diätetik
- Medizin | Veterinärmedizin Medizin | Public Health | Pharmazie | Zahnmedizin Klinische und Innere Medizin Endokrinologie
- Medizin | Veterinärmedizin Medizin | Public Health | Pharmazie | Zahnmedizin Klinische und Innere Medizin Stoffwechselstörungen
Weitere Infos & Material
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
11ß-Hydroxysteroid Dehydrogenase Type 1 (11ß-HSD-1) Enzyme and Obesity 61
Glucocorticoids and Perilipins 63
Glucocorticoids, TNF-a, and Inflammation 64
Perilipins, 11ß-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-ß, 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 ß 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 Infl