Metabolic Syndrome and Neurological Disorders

Name: Metabolic Syndrome and Neurological Disorders
Brand: Wiley-Blackwell
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Akhlaq A. Farooqui Tahira Farooqui(Herausgeber*in)

Wiley-Blackwell (Verlag)

Erschienen am 16. September 2013

576 Seiten

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Intro
METABOLIC SYNDROME AND NEUROLOGICAL DISORDERS
CONTENTS
FOREWORD
PREFACE
ACKNOWLEDGMENTS
CONTRIBUTORS
1 INSULIN RESISTANCE AND METABOLIC FAILURE UNDERLIE ALZHEIMER DISEASE
1.1 INTRODUCTION
1.2 MEDIATORS OF INSULIN SIGNALING
1.2.1 Insulin, the Master Hormone
1.2.2 Insulin-Stimulated Effects
1.2.3 Insulin-Like Growth Factors (IGFs)
1.2.4 Insulin and IGF Signaling in the Brain
1.2.5 Insulin and IGF Signal Transduction: Steps in Pathway Activation
1.2.6 Cross Talk between Insulin/IGF and Other Major Signal Transduction Networks in the Brain
1.3 INSULIN RESISTANCE AND NEURODEGENERATION
1.3.1 Insulin Resistance and Its Consequences
1.3.2 Alzheimer Disease (AD)
1.3.3 Concept: AD is a Metabolic Disease Driven by Brain Insulin/IGF Resistance
1.3.4 Brain Insulin and IGF Resistance and Deficiency in AD-Human Studies
1.3.5 AD = Type 3 Diabetes
1.3.6 Experimental Type 3 Diabetes (Sporadic AD)
1.4 THE NEUROPATHOLOGY OF AD IS CAUSED BY BRAIN INSULIN/IGF RESISTANCE
1.4.1 Overview
1.4.2 Tau Pathology
1.4.3 Amyloid-Beta (A PP-A )
1.4.4 Oxidative Stress
1.4.5 Endoplasmic Reticulum Stress
1.4.6 Metabolic Deficits-The Starving Brain
1.4.7 Chronic Ischemic Cerebral Microvascular Disease
1.5 BRAIN METABOLIC DERANGEMENTS IN OTHER NEURODEGENERATIVE DISEASES
1.6 UNDERLYING CAUSES OF BRAIN INSULIN RESISTANCE IN AD
1.6.1 Aging
1.6.2 Lifestyle-Induced Accelerated Aging
1.6.3 Peripheral Insulin Resistance Diseases
1.6.4 Nitrosamines and Insulin Resistance
1.6.5 Familial/Genetic Cofactors in the Type 3 Diabetes Aspects of AD
1.7 MECHANISTIC HYPOTHESES REGARDING AD PATHOGENESIS
1.7.1 Reverberating Mal-signaling Network
1.7.2 Extrinsic Factors Mediating Brain Insulin Resistance-the Liver-Brain Axis of Neurodegeneration
1.7.3 Intrinsic Pathway to Type 3 Diabetes
1.8 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
2 INSULIN RECEPTOR AND THE PATHOPHYSIOLOGY OF ALZHEIMER DISEASE
2.1 INTRODUCTION
2.2 INSULIN RECEPTOR SIGNALING PATHWAY
2.2.1 Insulin Receptor
2.2.2 Insulin Receptor Substrates (IRS)
2.2.3 SH2 Adaptor Proteins
2.2.4 PI3-Kinase Pathway
2.2.5 MAP-Kinase Pathway
2.3 INSULIN RECEPTOR SIGNALING IN THE BRAIN
2.3.1 Insulin Receptor Expression in the Brain
2.3.2 Insulin Transport Across the Blood Brain Barrier
2.3.3 Insulin Action in the Brain
2.4 INSULIN RECEPTOR AND ALZHEIMER DISEASE
2.4.1 Amyloid-
2.4.2 Tau
2.4.3 Insulin-Receptor Signaling in Alzheimer Disease
2.5 CONCLUSION
REFERENCES
3 CONTRIBUTION OF INSULIN RESISTANCE IN PATHOGENESIS OF ALZHEIMER DISEASE
3.1 INTRODUCTION
3.2 SYNOPSIS OF INSULIN SIGNALING RELATED WITH AD
3.2.1 mTORC1 Activation
3.2.2 mTORC2
3.2.3 Insulin Signaling in FOXO Regulation
3.2.4 DAPK/Pin1 Signaling Related with Insulin Transduction Pathway
3.3 WNT/ß-CATENIN SIGNALING LINKED WITH IR/AD
3.4 AMPK SIGNALING FOR THE ENERGY AND REDOX HOMEOSTASIS
3.5 ATM SIGNALING AS ANOTHER REDOX REGULATOR
3.6 SIRTUINS RELATED WITH IR/AD PATHOGENESIS
3.7 IMPORTANCE OF CDK5-CALPAIN INTERACTION IN IR/AD
3.8 AUTOPHAGY-LINKED TO IR/AD
3.9 OXIDATIVE STRESS IS IN THE VERY HEART OF IR/AD PATHOGENESIS
3.9.1 Angiotensin II and ROS
3.9.2 The Importance of Thioredoxin and Nucleoredoxin Systems in Oxidative Stress
3.9.3 Thioredoxin-Interacting Protein and Redox
3.9.4 Sirtuins in Oxidative Stress
3.9.5 FOXO in Oxidative Stress
3.9.6 Oxidative Stress and Calpain-Cdk5
3.10 A NOVEL INTEGRATING MODEL FOR IR AND AD
3.11 CONCLUSION
DEDICATION
REFERENCES
4 INSULIN-LEPTIN SIGNALING IN THE BRAIN
4.1 INTRODUCTION
4.2 LEPTIN- AND INSULIN-RELATED SIGNALING IN THE CENTRAL REGULATION OF ENERGY HOMEOSTASIS
4.3 CROSS-TALK BETWEEN INSULIN AND LEPTIN SIGNALING IN THE BRAIN
4.4 CENTRAL LEPTIN AND INSULIN RESISTANCE: CLINICAL IMPLICATIONS
4.4.1 Defective Intracellular Signaling and Metabolic Alterations
4.4.2 Leptin, Insulin, and Neurodegenerative Diseases
4.5 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
5 THE JANUS FACE OF INSULIN IN BRAIN
5.1 INTRODUCTION
5.1.1 Overview of the Labyrinth of Neuronal Insulin Receptor-Mediated Signaling Cascades
5.1.2 The Relevance of Insulin and IR in CNS
5.1.3 Insulin Neuroprotection against Chronic Effects of Diabetes
5.1.4 Insulin Neuroprotection against Age-Related Neurodegeneration and AD Pathology
5.1.5 Is There a Therapeutic Window for Insulin against Diabetes- and Age-Related Neurodegeneration?
5.2 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
6 MODULATION OF COGNITION BY INSULIN AND AGING: IMPLICATIONS FOR ALZHEIMER DISEASE
6.1 INTRODUCTION
6.2 INSULIN, INSULIN RECEPTOR SIGNALING, AND INSULIN ACTION IN THE BRAIN
6.2.1 Insulin Production, Insulin Receptor Distribution
6.2.2 Insulin Receptor Signaling
6.2.3 Insulin Actions in the Brain
6.3 BRAIN INSULIN RESISTANCE
6.3.1 Aging
6.3.2 Obesity and Peripheral Insulin Resistance
6.3.3 Cortisol and Cathecolamines
6.4 BRAIN INSULIN RESISTANCE AND PROTEIN ANORMALITIES
6.4.1 Impaired insulin signaling and Tau pathology in Alzheimer Disease
6.4.2 Insulin Resistance and Amyloid-Beta Neurotoxicity
6.5 BRAIN INSULIN RESISTANCE, OXIDATIVE STRESS, MITOCHONDRIAL DYSFUNCTION, AND INFLAMMATION IN AZHEIMER'S DISEASE
6.6 CONCLUSION
REFERENCES
7 CONTRIBUTION OF PHOSPHOLIPID, SPHINGOLIPIDS, AND CHOLESTEROL-DERIVED LIPID MEDIATORS IN THE PATHOGENESIS OF METABOLIC SYNDROME AND NEUROLOGICAL DISORDERS
7.1 INTRODUCTION
7.2 FATTY ACIDS IN METABOLIC SYNDROME
7.3 EICOSANOIDS AND OTHER ARACHIDONIC ACID-DERIVED METABOLITES IN METABOLIC SYNDROME
7.4 DIACYLGLYCEROLS IN METABOLIC SYNDROME
7.5 CERAMIDE IN METABOLIC SYNDROME
7.6 ENDOCANNABINOIDS IN METABOLIC SYNDROME
7.7 CHOLESTEROL AND OXY/HYDROXYSTEROL IN METABOLIC SYNDROME
7.8 FATTY ACIDS IN NEUROLOGICAL DISORDERS
7.9 EICOSANOIDS IN NEUROLOGICAL DISORDERS
7.10 4-HYDROXYNONENAL IN NEUROLOGICAL DISORDERS
7.11 DIACYLGLYCEROL IN NEUROLOGICAL DISORDERS
7.12 CANNABINOIDS IN NEUROLOGICAL DISORDERS
7.13 CERAMIDE IN NEUROLOGICAL DISORDERS
7.14 OXY/HYDROXYCHOLESTEROL IN NEUROLOGICAL DISORDERS
7.15 INTERACTIONS AMONG LIPID MEDIATOR IN METABOLIC SYNDROME AND NEUROLOGICAL DISORDERS
7.16 CONCLUSION
REFERENCES
8 LIPIDS, CHOLESTEROL, AND OXIDIZED CHOLESTEROL IN ALZHEIMER AMYLOID BETA-MEDIATED NEUROTOXICITY
8.1 INTRODUCTION
8.2 MODEL MEMBRANE SYSTEMS
8.3 AMYLOID BETA INTERACTION WITH MEMBRANES
8.4 AMYLOID BETA, CHOLESTEROL, AND MEMBRANE SYSTEMS
8.5 CHOLESTEROL OXIDATION
8.6 OXIDIZED CHOLESTEROL AND AMYLOID BETA
8.7 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
9 OF SOUND MIND AND BODY: DIETARY LIFESTYLES, PROMOTION OF HEALTHY BRAIN AGING, AND PREVENTION OF DEMENTIA IN HEALTHY INDIVIDUALS
9.1 INTRODUCTION
9.2 ALZHEIMER DISEASE DEMENTIA
9.2.1 Metabolic Syndrome and Its Role in Cognitive Deterioration During Aging as a Risk Factor for the Onset of AD Dementia
9.3 ROLE OF GRAPE-DERIVED POLYPHENOLS IN THE PREVENTION OF AD: A MODIFIABLE LIFESTYLE FACTOR DURING AGING
9.3.1 Preclinical DIM and Cognition
9.3.2 Multiple Polyphenol Preparations Have the Capacity to Directly or Indirectly Modulate DIM-Mediated Cognitive Deterioration
9.4 AD IS PREVENTABLE THROUGH MODIFIABLE LIFESTYLE INTEVENTIONS: PRIMARY, SECONDARY, AND TERTIARY INTERVENTIONS
9.4.1 Implications for a Combinatorial Approach for Treating DIM-Associated Cognitive Dysfunction
9.4.2 Bioavailability of Concord Grape Juice, GSE, and Resveratrol in the Brain
9.4.3 Bioactivities of Brain-Targeted Polyphenolic Components
9.5 EPIGENETIC MODIFICATIONS AND ITS ROLE IN DIABETES
9.5.1 Linking Epigenetic Modifications in Diabetes with Cognitive Impairments
9.6 CONCLUSION: THE FUTURE OF TRANSLATIONAL SCIENCE IN DIETARY LIFESTYLE APPLICATIONS AS A FUNCTION OF PATHOLOGICAL COGNITIVE DECLINE
ACKNOWLEDGMENTS
REFERENCES
10 METABOLIC SYNDROME AS AN INDEPENDENT RISK FACTOR OF SILENT BRAIN INFARCTION
10.1 INTRODUCTION
10.2 EPIDEMIOLOGY AND CHARACTERISTICS OF SBI
10.3 CLINICAL IMPACTS OF SBI
10.4 METABOLIC SYNDROME AND SBI: CURRENT EVIDENCES
10.5 POSSIBLE MECHANISMS OF SBI IN MetS
10.6 IS SBI REALLY SILENT?
10.7 CONCLUSION
REFERENCES
11 NEUROCHEMICAL LINKAGE AMONG METABOLIC SYNDROME, ALZHEIMER DISEASE, AND DEPRESSION
11.1 INTRODUCTION
11.2 METABOLIC SYNDROME IS AN INFLAMMATORY CONDITION
11.2.1 Cholinergic Anti-inflammatory Pathway in Metabolic Syndrome
11.3 VAGUS IS THE MESSENGER BETWEEN THE LIVER AND THE BRAIN
11.3.1 Vagus is the Messenger between Liver and Pancreatic Cells
11.4 HYPOTHALMIC NEUROPEPTIDES AND METABOLIC SYNDROME
11.5 HYPOTHALMIC INFLAMMATION OCCURS IN METABOLIC SYNDROME IN WHICH BDNF AND PUFAs HAVE A ROLE
11.6 ALZHEIMER DISEASE, BDNF, AND PUFA
11.7 OXIDATIVE STRESS AND INFLAMMATION IN AD
11.8 CHOLINERGIC SYSTEM AND AD
11.8.1 AD is an Inflammatory Condition
11.8.2 BDNF in AD
11.8.3 PUFAs in AD
11.9 PUFAs AND BDNF INTERACT WITH EACH OTHER
11.10 DEPRESSION IS A LOW-GRADE SYSTEMIC INFLAMMATORY CONDITION
11.11 PUFAs IN DEPRESSION
11.12 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
12 ALTERATIONS IN THE ENDOCANNABINOID SYSTEM AS A LINK BETWEEN UNBALANCED ENERGY HOMEOSTASIS, NEUROINFLAMMATION, AND NEUROLOGICAL AND NEUROPSYCHIATRIC DISORDERS
12.1 INTRODUCTION: THE ENDOCANNABINOID SYSTEM
12.2 ENDOCANNABINOID SYSTEM ALTERATIONS IN METABOLIC DISORDERS
12.3 ENDOCANNABINOID SYSTEM ALTERATIONS IN NEUROINFLAMMATION AND ALZHEIMER DISEASE
12.4 ENDOCANNABINOID SYSTEM ALTERATIONS IN STRESS, DEPRESSION AND PSYCHIATRIC DISORDERS
12.5 CONCLUSION
REFERENCES
13 METABOLIC SYNDROME, ALZHEIMER DISEASE, SCHIZOPHRENIA, AND DEPRESSION: ROLE FOR LEPTIN, MELATONIN, KYNURENINE PATHWAYS, AND NEUROPEPTIDES
13.1 INTRODUCTION
13.2 TRYPTOPHAN CATABOLITE (TRYCAT) PATHWAYS
13.3 LEPTIN AND TRYCATs
13.3.1 Leptin Resistance
13.3.2 Leptin Resistance, Decreased Leptin, and Neurodegeneration
13.3.3 Leptin, Leptin Resistance, and Melatonin
13.3.4 Wider Leptin and Melatonin Interactions
13.4 TREATMENT IMPLICATIONS
13.4.1 Acetylcholinesterase Inhibitors
13.4.2 Metformin
13.4.3 Leptin
13.4.4 Melatonin
13.5 CONCLUSION
REFERENCES
14 BINGE EATING AND METABOLIC SYNDROME
14.1 INTRODUCTION
14.2 DEMOGRAPHICS
14.3 EATING- AND WEIGHT-RELATED BEHAVIORAL CORRELATES
14.4 DIETING, BINGE EATING, AND METABOLIC SYNDROME
14.5 METABOLIC IMPACT OF BINGE EATING
14.6 EATING DISORDERS AND DEVELOPMENT OF METABOLIC SYNDROME
14.7 BRAIN AND ENERGY BALANCE
14.8 THE ROLE OF SOME PSYCHOPHYSIOLOGICAL MECHANISMS
14.9 CONCLUSION
REFERENCES
15 PHYTOCHEMICAL PRINCIPLES IN THE TRADITIONAL INDIAN SYSTEM OF MEDICINE USED FOR THE MANAGEMENT OF METABOLIC SYNDROME
15.1 INTRODUCTION
15.2 ROLE OF MEDICINAL PLANTS IN THE MANAGEMENT OF METABOLIC SYNDROME
15.2.1 Jamun
15.2.2 Bijasar
15.2.3 Karela
15.2.4 Methi
15.2.5 Tulsi
15.2.6 Lahsun
15.2.7 Onion
15.3 CONCLUSION
REFERENCES
16 OXIDATIVE STRESS AND OBESITY: THEIR IMPACT ON METABOLIC SYNDROME
16.1 INTRODUCTION
16.2 OBESTY AND OXIDATIVE STRESS IN ADIPOSE TISSUE
16.3 OXIDATIVE STRESS AND ADIPOCYTOKINES
16.4 OVERNUTRITION AND OXIDATIVE STRESS
16.5 OXIDATIVE STRESS AND INSULIN RESISTANCE
16.6 SYSTEMIC OXIDATIVE STRESS AND METABOLIC SYNDROME
16.7 OXIDATIVE STRESS AND CLINICAL TREATMENTS
REFERENCES
17 THE RELATIONSHIP AMONG OBESITY, INFLAMMATION, AND INSULIN RESISTANCE
17.1 INTRODUCTION
17.2 INFLAMMATION IN OBESITY
17.2.1 Adipose Tissue Inflammation and Macrophages Infiltration
17.2.2 Adipose Tissue Inflammation and Other Immune Cells Infiltration
17.3 INFLAMMATION AND INSULIN RESISTANCE PATHWAYS
17.3.1 Cytokine Pathways
17.3.2 Adipokine Involvement
17.4 ENDOPLASMIC RETICULUM STRESS AND INSULIN RESISTANCE
17.5 THE ROLE OF THE COMMENSALLY FLORA OR MICROBIOTA IN THE METABOLIC INFLAMMATION
17.6 CONCLUSION
REFERENCES
18 INVOLVEMENT OF ADIPOCYTOKINES IN PATHOGENESIS OF INSULIN RESISTANCE, OBESITY, AND METABOLIC SYNDROME
18.1 INTRODUCTION
18.2 ADIPONECTIN
18.2.1 Experimental and Clinical Data on Adiponectin
18.2.2 Therapeutic Strategies
18.3 RESISTIN
18.3.1 Mechanisms of Action
18.3.2 Epidemiological Evidence in Humans
18.4 RETINOL-BINDING PROTEIN 4 (RBP4)
18.4.1 RBP4: Experimental Data
18.4.2 RBP4 in Metabolic Syndrome: Clinical Studies
18.5 LEPTIN
18.5.1 Pro-inflammatory Roles of Leptin
18.5.2 Potential Use of Leptin in Therapy
18.6 VISFATIN
18.7 THERAPEUTIC INTERVENTIONS IN RELATION TO ADIPOCYTOKINES
ACKNOWLEDGMENTS
REFERENCES
19 OBESITY, INFLAMMATION, AND VASCULAR DISEASE: NOVEL INSIGHT IN THE ROLE OF ADIPOSE TISSUE
19.1 INTRODUCTION
19.2 ADIPOSE TISSUE AS AN ENDOCRINE ORGAN
19.3 ADIPOCYTOKINE AND CARDIOVASCULAR RISK
19.3.1 Leptin
19.3.2 Adiponectin
19.3.3 Resistin
19.3.4 C-Reactive Protein
19.4 EFFECTS OF WEIGHT LOSS
19.5 CONCLUSION
REFERENCES
20 IS DIABETES A RISK FACTOR FOR PARKINSON DISEASE?
20.1 INTRODUCTION
20.2 PARKINSON DISEASE
20.3 TYPE 2 DIABETES
20.4 IS THERE ANY MOLECULAR LINK BETWEEN TYPE 2 DIABETES AND PARKINSON DISEASE?
20.5 CONCLUSION
REFERENCES
21 ROLE OF IRON IN THE PATHOGENESIS OF DIABETES AND METABOLIC SYNDROME
21.1 INTRODUCTION
21.2 IRON HOMEOSTASIS, BIOLOGICAL FUNCTION AND TOXICITY
21.2.1 Iron Homeostatic Regulation
21.2.2 Biological Functions of Iron
21.2.3 Chemical Features and Toxicity of Iron
21.3 IRON DEFICIENCY
21.3.1 Iron Deficiency, Glycated Hemoglobin Levels, and Insulin Resistance
21.3.2 Blood Donation, Insulin Sensitivity, and Cardiovascular Diseases
21.3.3 Cautions for the Diabetic Patients to Donate the Blood
21.4 IRON OVERLOAD
21.4.1 Iron Overload and Insulin Resistance or Type 2 Diabetes
21.4.2 Iron Overload and Type 1 or Gestational Diabetes
21.4.3 Iron Overload and Diabetic Complications
21.5 POSSIBLE MECHANISMS BY WHICH IRON INVOLVES IN THE PATHOGENESIS OF DIABETES AND DIABETIC COMPLICATIONS
21.5.1 Advanced Glycated Endproducts
21.5.2 Iron Enhancement of the Pathological Effects of Angiotensin II
21.5.3 HO-1
21.5.4 An Interaction Between Iron and Retinol-Binding Protein
21.5.5 Hepcidin
21.5.6 Others
21.6 POSSIBLE THERAPY FOR DIABETES AND DIABETIC COMPLICATIONS USING IRON CHELATORS
21.7 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
22 CONTRIBUTIONS OF AMP KINASE TO THE PATHOGENESIS OF TYPE 2 DIABETES AND NEURODEGENERATIVE DISEASES
22.1 INTRODUCTION
22.2 BACKGROUND
22.2.1 Organization of AMPK
22.3 AMPK AND HUMAN HEALTH
22.3.1 AMPK in the Pancreas
22.3.2 AMPK in Skeletal Muscle
22.3.3 AMPK in the Liver
22.3.4 AMPK in Adipose Tissue
22.3.5 AMPK in the Nervous System
22.4 DIABETES MODULATES FUNCTIONS OF THE NERVOUS SYSTEM
22.5 AMPK AND NEURODEGENERATIVE DISEASES
22.5.1 AMPK in Alzheimer Disease
22.5.2 AMPK in Huntington Disease
22.5.3 AMPK in Parkinson Disease
22.6 CONCLUSION: AMPK-A COMMON MOLECULAR TARGET FOR THE TREATMENT OF DIABETES AND NEURODEGENERATIVE DISEASES?
ACKNOWLEDGMENTS
REFERENCES
23 A DEPOSITION, INSULIN SIGNALING, AND TAU PHOSPHORYLATION IN ANIMAL MODELS OF ALZHEIMER DISEASE AND DIABETES
23.1 INTRODUCTION
23.2 AD AND DIABETES
23.3 AD MODELS WITH DIABETES
23.3.1 Amyloid Burden in AD Models with Diabetes
23.3.2 Insulin Signaling in AD Model with Diabetes
23.3.3 Tau Phosphorylation in AD Model with Diabetes
23.3.4 Impaired Diabetic Phenotype in AD Model with Diabetes
23.4 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
24 IN VIVO EVIDENCE OF THE CONVERGENCE OF TYPE 2 DIABETES AND ALZHEIMER DISEASE
24.1 INTRODUCTION
24.2 STUDIES IN DIABETES MELLITUS MODELS (TABLE 24.1)
24.2.1 Streptozotocin-Injection Models
24.2.2 Spontaneous DM Models
24.2.3 Genetic Models Targeting Insulin Signaling
24.3 STUDIES WITH AD MODELS (TABLE 24.2)
24.3.1 The effect of STZ injection in transgenic mouse models of AD
24.3.2 Transgenic Mouse Models of AD with a High-Calorie-Diet Induced T2DM
24.3.3 Double-Transgenic Models of AD and T2DM
24.3.4 Genetic Modulation of Insulin Signaling in Transgenic AD Models
24.4 THERAPEUTIC TRIALS WITH ANTI-DIABETIC AGENTS WITH AD MODELS (TABLE 24.3)
24.5 CONCLUSION
24.6 ACKNOWLEDGMENTS
REFERENCES
25 METABOLIC SYNDROME AND ITS IMPACT ON CARDIOVASCULAR DISEASE
25.1 INTRODUCTION
25.2 BRIEF HISTORY OF METABOLIC SYNDROME
25.3 BRIEF OVERVIEW OF THE ATHEROSCLEROSIS MECHANISMS
25.4 METABOLIC SYNDROME AND THE RISK OF CARDIOVASCULAR DISEASE
25.5 ATHEROSCLEROSIS ORIGINATES IN OUR YOUTH
25.6 FEATURES OF METABOLIC SYNDROME AND THEIR IMPACT ON ATHEROSCLEROSIS DEVELOPMENT
25.6.1 Inflammation
25.6.2 Insulin Resistance and Hyperglycemia
25.6.3 Dyslipidemia
25.6.4 Hypertension
25.6.5 Hypercoaguable State
25.7 IS METABOLIC SYNDROME A USEFUL CONCEPT WHEN IT COMES TO CARDIOVASCULAR DISEASE PREVENTION?
25.8 CONCLUSION
REFERENCES
26 CONTRIBUTION OF INFLAMMATION, ADIPONECTIN, AND OBESITY IN CARDIOVASCULAR DISEASES
26.1 INTRODUCTION
26.2 ATHEROSCLEROSIS
26.2.1 Early Phase
26.2.2 Perpetuation and Advanced Phase
26.2.3 Atherosclerosis-Effector Cells
26.2.4 Atherosclerosis-Lipoproteins oxidized-LDL)
26.3 ADIPONECTIN
26.3.1 Physiologic Functions
26.3.2 Adiponectin in Obesity
26.3.3 Adiponectin and Cardiovascular Risk
26.4 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
27 BRAIN AND CARDIOVASCULAR DISEASES: MOLECULAR ASPECTS
27.1 INTRODUCTION
27.2 NEUROANATOMY AND NEUROCHEMISTRY OF THE CARDIOVASCULAR REGULATION
27.2.1 Distribution of the Cardiovascular Neurons
27.2.2 Neurochemical Regulation of the Cardiovascular Neurons
27.3 CONVENTIONAL NEUROTRANSMITTERS
27.3.1 Catecholamines
27.3.2 Glutamate and GABA
27.4 NONCONVENTIONAL NEUROTRANSMITTERS
27.4.1 Neuropeptides
27.4.2 Steroids, Ouabain-Like Factor and Other Factors
27.5 DISTURBANCES IN CARDIOVASCULAR REGULATION
27.5.1 Acute and Chronic Stress
27.5.2 Obesity
27.6 CENTRAL REGULATION OF THE CARDIOVASCULAR SYSTEM IN THE CARDIOVASCULAR DISEASES
27.6.1 Hypertension
27.6.2 Heart Failure
27.6.3 Cerebral Hypoxia and Ischemia
27.6.4 Intracranial Hemorrhage and Stroke
27.6.5 Degenerative Neurological Diseases
27.7 CONCLUSION
ACKNOWLEDGMENT
REFERENCES
28 MOLECULAR ASPECTS OF DIETARY-EXERCISE REGIMEN FOR THE PREVENTION OF METABOLIC SYNDROME
28.1 INTRODUCTION
28.2 EVIDENCE FOR THE BENEFICIAL EFFECTS OF EXERCISE
28.2.1 Molecular Mechanisms of Improvement in Metabolism Inside Muscle Induced By a Single Bout of Exercise
28.2.2 Molecular Mechanisms of Muscle Adaptative Benefits Induced By Regular Exercise
28.3 THE EFFECT OF EXERCISE ON METABOLIC CAPACITY IN OTHER METABOLIC ORGANS
28.4 CONCLUSION
REFERENCES
29 GHRELIN, LIPID METABOLISM, AND METABOLIC SYNDROME
29.1 INTRODUCTION
29.2 GHRELIN: A STOMACH-DERIVED PEPTIDE MODULATING ENERGY BALANCE
29.3 GHRELIN EFFECTS ON FOOD-INTAKE ARE MEDIATED BY THE OREXIGENIC NPY/AGRP NEURONS
29.4 TRANSCRIPTIONAL MACHINERY MEDIATING THE HYPOTHALAMIC ACTIONS OF GHRELIN
29.5 HYPOTHALAMIC FATTY ACID METABOLISM AND AMPK MEDIATE GHRELIN'S ACTIONS ON FOOD INTAKE
29.6 GHRELIN AND THE HYPOTHALAMIC SIRTUIN1 (SIRT1)/P53 AXIS
29.7 DOES GHRELIN ACT ON ALTERNATIVE CANONICAL ENERGY SENSORS BESIDES AMPK AND SIRT1?
29.8 CENTRAL GHRELIN ACTIONS ON PERIPHERAL LIPID METABOLISM
29.9 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
30 LEPTIN AND COGNITIVE FUNCTION
30.1 INTRODUCTION
30.2 LEPTIN
30.3 LEPTIN EXPRESSION IN THE BRAIN
30.4 LEPTIN RECEPTOR
30.4.1 Leptin Receptor Expression in the CNS
30.4.2 Leptin Receptor Signaling
30.5 SUPPRESSOR OF CYTOKINE SIGNALING (SOCS)-3
30.6 THE mTOR PATHWAY
30.7 LEPTIN TRANSPORT TO THE BRAIN
30.8 LEPTIN REGULATION OF HIPPOCAMPAL FUNCTION
30.8.1 Leptin Regulation of Hippocampal Synaptic Plasticity
30.8.2 Leptin Induces a Novel Form of Hippocampal LTD
30.8.3 Leptin Reverses Established LTP
30.8.4 Regulation of NMDA Receptor Function by Leptin
30.8.5 Regulation of AMPA Receptor Trafficking
30.8.6 Rapid Morphological Changes Induced By Leptin
30.9 LEPTIN AND DEVELOPMENT
30.10 LEPTIN AND AGING
30.11 LEPTIN AND NEURODEGENERATIVE DISORDERS
30.12 LEPTIN AND NEUROPROTECTION
30.13 LEPTIN AND AMYLOID BETA
30.14 CONCLUSION
ACKNOWLEDGMENTS
REFERENCES
31 FRUCTOSE, SUGAR CONSUMPTION, AND METABOLIC DISEASES
31.1 INTRODUCTION
31.2 FOOD ENERGY: THE ROLE OF THE LIVER IN PROCESSING ENERGETIC SUBSTRATES
31.3 SPLANCHNIC FRUCTOSE METABOLISM
31.4 METABOLIC EFECTS OF HIGH FRUCTOSE DIETS IN ANIMAL MODELS
31.5 EFFECTS OF FRUCOSE ON HUMAN HEALTH
31.6 FRUCTOSE AND HUMAN OBESITY
31.7 EFFECT OF FRUCTOSE ON BLOOD LIPIDS IN HUMANS
31.8 FRUCTOSE AND NONALCOHOLIC FATTY LIVER DISEASE
31.9 EFFECTS OF FRUCTOSE ON INSULIN SENSITIVITY AND GLUCOSE HOMEOSTASIS
31.10 EFFECTS OF FRUCTOSE ON BLOOD PRESSURE AND URIC ACID CONCENTRATIONS
31.11 EFFECTS OF FRUCTOSE ACCORDING TO GENDER
31.12 CONCLUSION
REFERENCES
32 INFLAMMATION-MEDIATED COGNITIVE AND EMOTIONAL ALTERATIONS IN EXPERIMENTAL MODELS OF METABOLIC SYNDROME
32.1 INTRODUCTION
32.2 METABOLIC SYNDROME AND NEUROPSYCHIATRIC SYMPTOMS
32.3 ANIMAL MODELS OF METABOLIC SYNDROME
32.3.1 Modeling Metabolic Syndrome in Rodents
32.3.2 Cognitive and Emotional Alterations in Rodent Models of Metabolic Syndrome
32.4 MECHANISMS UNDERLYING THE ASSOCIATION BETWEEN METABOLIC SYNDROME AND NEUROPSYCHIATRIC SYMPTOMS
32.5 INFLAMMATION, SICKNESS BEHAVIOR, AND NEUROPSYCHIATRIC SYMPTOMS
32.5.1 From Acute Sickness Behavior to Chronic Neuropsychiatric Symptoms
32.5.2 Mechanisms Linking Cytokine-Induced Brain IDO Activation and Neuropsychiatric Symptoms
32.6 ROLE OF INFLAMMATION IN EMOTIONAL AND COGNITIVE ALTERATIONS ASSOCIATED WITH METABOLIC SYNDROME
32.6.1 Metabolic Syndrome: A Peripheral and Brain Inflammatory Disorder
32.6.2 Relevance of Metabolic Syndrome-Associated Inflammation for Emotional and Cognitive Alterations and Underlying Mechanisms
32.7 CONCLUSION
REFERENCES
33 SUMMARY AND PERSPECTIVE
33.1 INTRODUCTION
33.2 EFFECT OF DIET ON MetS AND NEUROLOGICAL DISORDERS
33.3 NEUROCHEMICAL LINKS BETWEEN MetS AND NEUROLOGICAL DISORDERS
33.4 CONCLUSION
REFERENCES
INDEX

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