Obesity

Authors: Manuel Serrano Ríos, J.M. Ordovas, Jose A. Gutiérrez Fuentes Publisher: Elsevier Health Sciences Spain Publication date: 2011 Publication language: Angielski Number of pages: 397 Publication formats: EAN: 9788480865364 ISBN: 9788480865364 Category: Neurology & clinical neurophysiology Publisher's index: 9788480865364 Bibliographic note: -

Description

• "Obesity" es el segundo libro de una colección de cuatro ("Type 2 diabetes mellitus (T2D)"; "Obesity"; "Arterial hypertension"; "Atherogenic dyslipidemia").
• Se trata de una obra realizada con un enfoque multidisciplinar y producto del trabajo realizado por un equipo de colaboradores internacionales de gran prestigio en las distintas áreas, escrita íntegramente en inglés, revisa todos los aspectos relacionados con la obesidad.
• Abarca desde los aspectos generales como la obesidad en niños y su impacto en la sanidad pública, factores sociales, demográficos y económicos, su relación con la diabetes o la importancia de la genética, hasta la fisiopatología, prevención y las distintas opciones de tratamiento farmacológico, psicológico, e importancia de la actividad física.

• "Obesity" es el segundo libro de una colección de cuatro ("Type 2 diabetes mellitus (T2D)"; "Obesity"; "Arterial hypertension"; "Atherogenic dyslipidemia").
• Con un enfoque multidisciplinar, está escrita íntegramente en inglés y revisa todos los aspectos relacionados con la obesidad.
• Abarca desde los aspectos generales como la obesidad en niños y su impacto en la sanidad pública, hasta la fisiopatología, prevención y las distintas opciones de tratamiento.

TOC

• Front Cover 2
• Front Matter 3
• Copyright 6
• Contents 7
• Contributors 9
• Preface 11
• Section I : General Aspects 13
• Chapter 1 - Leptin and the regulation of body weight 15
  • Abstract 15
  • Introduction 15
  • Key words 15
  • Historical background 16
  • The cloning of the ob gene and identification of leptin has uncovered a new endocrine system regulating body weight 17
  • Changes in nutritional state regulate other physiologic systems 20
  • Many leptin deficiency syndromes are treatable with leptin replacement 22

• Front Cover 2
• Front Matter 3
• Copyright 6
• Contents 7
• Contributors 9
• Preface 11
• Section I : General Aspects 13
• Chapter 1 - Leptin and the regulation of body weight 15
  • Abstract 15
  • Introduction 15
  • Key words 15
  • Historical background 16
  • The cloning of the ob gene and identification of leptin has uncovered a new endocrine system regulating body weight 17
  • Changes in nutritional state regulate other physiologic systems 20
  • Many leptin deficiency syndromes are treatable with leptin replacement 22
  • Most obese patients are leptin resistant 24
  • Biologic basis for obesity 26
  • Leptin provides an entry point for studying a complex human behavior 26
• Chapter 2 - Obesity: A modern pandemic 31
  • Key words 31
  • Introduction: The evolution of medical and nutritional thinking 31
  • Standardising the approach to the measurement of "normal" body weight and obesity 32
  • Obesity becomes recognised as a public health problem 33
  • Estimating childhood obesity 34
  • The global prevalence of obesity 34
  • Children's prevalences of overweight and obesity 36
  • The burden of disease: Obesity ranks near the top! 38
  • Optimum BMIs For longevity are <25 and for a disease-free life 20? 41
  • The proportion of different adult diseases attributable to excess weight 41
  • Disease costs of obesity 42
  • Epidemiological analyses relating to the promotion of obesity 43
  • Acknowledgements 45
• Chapter 3 - Developmental origins of childhood obesity: Potential public health impact 47
  • Introduction 47
  • Prenatal Period 47
  • Postnatal Period (Birth to 5 Years) 49
    • Rapid Infant Weight Gain 49
    • Breastfeeding 51
    • Sleep Duration 52
    • Parenting Practices Relating to Food and Physical Activity 53
  • Summary 54
• Chapter 4 - Genetics of Obesity:Are Genetic DifferencesContributing to theObesity Epidemic? 59
  • Introduction 59
  • Single Genes Causing Obesity 60
  • Mendelian Disorders 60
  • Single-Gene Nonsyndromic Disorders 61
  • Leptin and Leptin Receptor Genes 62
  • Proopiomelanocortin (POMC) Gene Defi ciencies 63
  • Melanocortin 4 Receptor (MC4R) Gene 63
  • Familial Risk Level, Heritability and Tracking 64
  • Prohormone Convertase 1 (PCSK1 or PC1) 64
  • Polygenes and the Risk of Obesity 64
  • Oligogenes and Polygenes 65
  • Genes with Small Effects 65
  • Gene-Nutrition and Gene-Physical Activity Interactions 68
  • Genetic Variation and the Obesity Epidemic 70
  • Conclusions 71
  • References 72
• Chapter 5 - Social, demographic, and economic status factors and obesity: A global perspective 77
  • Key words 77
  • Introduction 77
  • Between-country variation in the prevalence and trend 78
  • Gender differences 83
  • Age differences 85
  • Ethnic differences within countries 85
  • Socioeconomic status (SES) measures and obesity 86
  • Rural/Urban differences 92
  • Discussion and conclusions 95
  • Acknowledgements 96
• Chapter 6 - The adipose tissue: From a passive fat depot to an active endocrine organ 99
  • Key words 99
  • Introduction 99
  • Developmental origin of adipose tissue 99
    • Adipogenesis 100
    • White adipocyte dynamics 100
  • Structural characteristics 102
  • Depot-specific differences and fat distribution 104
  • Physiological functions and pathophysiology 104
  • Future prospects and concluding remarks 116
• Chapter 7 - Endocrine Regulationof Energy Homeostasis:Implications forObesity and Diabetes 119
  • Introduction and Overview 119
  • Short-Term vs. Long-Term Regulation of Energy Homeostasis 120
  • Gastrointestinal Hormones 123
    • Ghrelin 123
    • Glucose-Dependent Insulinotropic Polypeptide (GIP) 124
    • Glucagon-Like Peptide-1 (GLP-1) 124
    • Oxyntomodulin 125
    • Peptide-YY (PYY3-36) 126
  • Adipocyte Hormones 126
    • Leptin 126
    • Adiponectin 127
  • Dietary Macronutrients and the Endocrine Regulation of Energy Balance 129
  • Summary 131
• Section II : Physiopathology 139
• Chapter 8 - Gene-Diet interactions and obesity 141
  • Key words 141
  • Introduction 141
  • Obesity as a modulating phenotype of the effect of the genetic variants 142
  • Gene-environment interactions and obesity-related traits 143
  • Statistical methods for gene-environment interactions 144
  • Summary 145
  • Acknowledgements 152
• Chapter 9 - Neuroendocrine regulation of food intake and body weight 157
  • Key Words 157
  • Abstract 157
  • Introduction 157
  • The Link between the Periphery and the Brain 158
  • The Melanocortin System and Long-Term Energy Balance 160
  • Modulation of Melanocortin Circuits from the VMH 162
  • The Lateral Hypothalamic Arousal/Feeding System 163
  • Midbrain Dopamine System: The Motivation or Incentive to Eat 164
  • Other Hypothalamic Regions that Regulate Food Intake and Body Weight 165
  • The Caudal Brainstem: Autonomic Control of Eating 165
  • Neuronal Responses to Peripheral Hormones 166
    • Acute Neuronal Responses to Peripheral Hormones 166
    • Synaptic Plasticity Driven by Peripheral Metabolic Hormones 167
  • Fuel Sensing and Energy Balance 169
  • Summary of Thoughts 171
• Chapter 10 - Obesity, inflammation and the metabolic syndrome 181
  • Key words 181
  • Introduction 181
  • History of Obesity-Associated Inflammation 181
    • History 181
    • Character 182
  • Inflammation Mediators and Macrophages 182
    • Inflammation Mediators 182
      • Systemic Insulin Resistance 185
      • Fuel Mobilization 185
      • Adipocyte Inhibition 185
      • Energy Balance 185
    • Macrophages 186
      • Macrophage Types 186
      • Mechanism of Macrophage Infiltration 186
      • Biological Significance 187
    • Tissue-Specific Inflammation 187
      • Adipose Tissue 187
      • Liver Inflammation 188
      • Skeletal Muscle Inflammation 188
    • Inflammation Signaling Pathways 189
      • IKK2/NF-kB Pathway 189
      • JNK/AP1 Pathway 190
      • JAK/STAT Pathway 190
    • Origin of Obesity-Associated Inflammation 191
      • Lipids 191
      • Hypoxia 191
      • Endoplasmic Reticulum Stress 191
      • Oxidative Stress 192
    • Inflammation in Insulin Resistance 192
      • IRS-1 Inhibition 192
      • PPARγ Inhibition 192
    • Inflammation in Chronic Diseases 193
      • Type 2 Diabetes 193
      • Hypertension 193
    • Anti-Inflammation System in Obesity 194
      • Adiponectin 194
      • IL-1Ra 194
      • IL-10 195
    • Chapter 11 - Obesity and the liver. Pathophysiological implications 201
      • Why Has the Liver Been a Forgotten Organ in Obesity and Insulin Resistance? 201
      • Abstract 201
      • NAFLD and Metabolic Syndrome Definitions 202
      • Hypertriglyceridemia and Low HDL Cholesterol and Liver Fat 203
      • Fasting Hyperinsulinemia and Hyperglycemia and Liver Fat 203
      • Measurement of Liver Fat Content 205
      • Genetic Variation in PNPLA3 (adiponutrin) Influences Liver Fat but not Components of the Metabolic Syndrome 205
      • When Should NASH be Suspected in an Obese Subject with a Fatty Liver? 206
      • Sources of Excessive Intrahepatocellular Triglycerides 206
        • Role of Lipolysis and Features of Insulin Resistance in Adipose Tissue 206
        • Role of de Novo Lipogenesis 207
      • Liver Fat and Obesity - Clinical Significance 208
        • Acknowledgements 208
      • Chapter 12 - Fat tissue and cardiovascular diseases. The fat connection 213
        • Fatness Going Wild 213
        • Adipose Tissue and Vascular Disease 214
        • Obesity, Fat and Endothelial Dysfunction 215
        • Fat and Inflammation 216
        • Body Fat, Perivascular Fat, and Oxidative Stress 217
        • Heart Disease and Epicardial Fat: An Enemy from Inside 218
        • The Bone Marrow: From Stemness to Fatness 219
          • Conclusions 221
        • Chapter 13 - Obesity and Type 2 Diabetes Mellitus. The reciprocal impact 227
          • Key words 227
          • Obesity and Type 2 Diabetes Mellitus 227
            • Background 227
            • An Epidemiological Perspective 227
          • Pathophysiological Perspectives: The Road from Obesity to Type 2 Diabetes Mellitus. Potential Mechanisms 229
            • The Free Fatty Acids Overflow Hypothesis and its Relationship to Insulin Resistance in Obesity 230
            • The Ectopic Fat Storage Hypothesis and the Concept of Tissue Lipotoxicity 231
            • The Endoplasmic Reticulum and the Mitochondria: Selective Intracellular Targets 235
              • The Endoplasmic Reticulum 235
              • The Mitochondria 236
            • Obesity, Inflammation and Insulin Resistance 238
              • The Consequences of Obesity-Associated Inflammation 239
              • Origin and Progress of Low-Grade Inflammation in Obesity 239
            • Summary 242
          • Chapter 14 - Fat tissue, thrombosis and atherosclerosis 245
            • Key words 245
            • Introduction 245
            • Fat Tissue and Atherosclerosis 245
              • Progression of Atherosclerosis 245
              • Fat Tissue Dysfunction in Obesity and Development of Atherosclerosis 246
                • Free Fatty Acids 246
                • Adiponectin 248
                • Inflammatory Mediators 248
              • Obesity and Thrombosis 249
                • Obesity and Endothelial Dysfunction 249
                • Obesity and the Coagulation/Fibrinolytic System 250
                • Platelet Function Modifications in Obesity 252
                • Antiplatelet Treatment in the Obese 253
              • Concluding Remarks 253
            • Section III : Prevention And Treatment 257
            • Chapter 15 - Current guidelines on the identification, evaluation, and treatment of overweight and obesity 259
              • Key words 259
              • Introduction 259
              • Identification of Obesity 259
              • Guidelines for Evaluation 260
                • Information from the Clinical Interview 260
                • Information from Physical Evaluation 260
                  • Step 1: Measure Body Mass Index 260
                  • Step 2: Measure Waist Circumference 260
                  • Other Aspects of the Physical Examination of Obesity 265
                • Information from Laboratory Tests 267
                  • Plasma Lipids 267
                  • Plasma Glucose 267
                  • Thyroid-Stimulating Hormone (TSH) 268
                  • Prostate-Specific Antigen (PSA) 268
                • Specialized Tests 268
                  • Ultrasound of the Gallbladder 268
                  • Electrocardiograms and Echocardiography 268
                  • Sleep Study 268
                  • Mammography 268
                • The Metabolic Syndrome 269
              • Guidelines for Treatment 269
                • Do Patient and Doctor Have Realistic Expectations? 271
                • Is the Patient Ready to Lose Weight? 271
                • Quality of Life 273
              • The Realities of Overweight 273
              • Guidelines for Treatment by Age Group 274
                • Age 1-10 Years 274
                • Age 11-50 Years 275
                • Age Over 51 Years 276
              • Conclusions 277
            • Chapter 16 - Prevention of child and adolescent overweight and obesity 279
              • Introduction 279
              • Existing state of obesity prevention knowledge 279
              • Key words 279
              • Mediating-moderating variable model (MMVM) as an organizing framework 280
                • Sources of mediating variables 281
              • Multiple influences on children's diet and physical activity 282
                • Awareness of need to change 282
                • Specific knowledge of behavior to change 283
                • Changes in Proximal Physical Environment to Support Behavior Change 284
                • Changes in Social Environment to Support Behavior Change 284
                • Motivation to learn knowledge or skills 284
                • Skills at overcoming barriers to change 285
                • Skills at mitigating anticipated negative emotions 285
                • Skills at performing behaviors 285
                • Habit 286
                • Resources Needed for Change 286
              • Next step: Optimal procedures for inducing change 286
              • Conclusions 287
            • Chapter 17 - The Role of PhysicalActivity and SedentaryBehavior on Obesity 291
              • Introduction 291
                • Energy Balance 291
                • Energy Gap 292
              • Assessment of Physical Activity in Populations 292
              • Accelerometry 293
              • Self-Reported Physical Activity 293
              • Objective Measurement of Physical Activity 293
              • Heart Rate Monitoring 294
              • Secular Decline in Population Levels of Physical Activity? 294
              • Do Higher Levels of Physical Activity Prevent Weight Gain? 296
              • Associations Between Self-Reported Physical Activity and Gain in Body Weight 296
              • Associations Between Objectively Measured Physical Activity and Gain in BodyWeight 298
              • Does Sedentary Behavior Promote Weight Gain? 301
              • The Issue of Reverse or Bidirectional Causality 303
              • Physical Activity Guidelines for Preventing Weight Gain 304
            • Chapter 18 - Obesity treatment: The use of exercise and behavioral strategies 309
              • Introduction 309
              • Key words 309
              • The role of exercise in obesity treatment 310
              • Factors contributing to exercise adherence 310
              • Development of the exercise prescription for weight control and adherence 311
                • Exercise mode 311
                • Physical activity volume: Intensity vs. duration 312
              • Behavioral strategies for exercise adoption and maintenance 313
                • Using self-monitoring, feedback, goal-setting, and contracts 314
                • Self-efficacy for exercise 314
                • Program tailoring: Stage-matching exercise intervention based on the transtheoretical model 315
                • Overcoming barriers to physical activity 316
                  • Lack of convenience 316
                  • Lack of time 316
                  • Lack of enjoyment 317
                • Social support 316
                • Intermittent physical activity 317
              • Summary 317
            • Chapter 19 - Lifestyle approaches to obesity treatment 323
              • Overview of lifestyle treatment 323
              • Key words 323
              • Evidence for the effectiveness of lifestyle intervention 324
                • Diabetes prevention study 325
                • Look AHEAD 326
                • Diabetes prevention program 326
              • Key intervention components 324

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Author's affiliation

J.M. Ordovas: Nutrition and Genomics Laboratory, USDA Human