Diabetes mellitus research advances /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Huber, Maximilian N.
Formato: Electrónico eBook
Idioma:Inglés
Publicado: New York : Nova Science Publishers, 2008.
Temas:
Diabetes.
Diabetes
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Intro
  • DIABETES MELLITUS RESEARCH ADVANCES
  • DIABETES MELLITUS RESEARCH ADVANCES
  • Contents
  • Preface
  • Chapter 1 The Metabolic Syndrome: Genetic Effects in Endocrine Pathways
  • Abstract
  • 1. Introduction
  • 2. The Metabolic Syndrome: Concept, Definition, Effect and Prevalence
  • 3. Pathophysiology of the Metabolic Syndrome
  • 4. Causes of the Metabolic Syndrome: Genetics and Environment
  • 5. Genetic Analysis of the Metabolic Syndrome
  • 5.1. Direct Methods (Based on Molecular Biology)
  • 5.1.1. Comparative Genomics
  • 5.1.2. Pharmacological Methods and Pharmacogenetics
  • 5.1.3. Other Functional Studies
  • 5.2. Indirect Methods (Based on Statistical Genetics)
  • Study design and genetic models
  • 5.2.1. Linkage Analysis
  • 5.2.2. Association Analysis
  • 5.2.3. Genome-Wide Scans
  • 5.2.4. Meta-analysis
  • 5.2.5. From Candidate Variants to Causal Variants
  • 5.2.6. Multilocus Approaches and Network Analyses
  • 5.3. Mixed Methods (Combining Molecular Biology and Statistical Genetics)
  • 6. Genetic Variants in Endocrine Pathways Influencing Metabolic Syndrome
  • 6.1. Central Nervous System Pathways
  • 6.1.1. Melanocortin/Agouti System
  • POMC (Pro-opiomelanocortin)
  • CART (Cocaine and Amphetamine-Regulated Transcript)
  • NPY (Neuropeptide Y)
  • Brain-derived Neurotrophic Factor (BDNF)
  • AgRP (Agouti-Related Peptide)
  • 6.1.2. GH-IGF axis
  • GH (Growth hormone)
  • IGF (Insulin-like growth factors)
  • IGF2
  • IGF1
  • 6.1.3. Metabolic Syndrome and Circadian Phenomenon
  • 6.2. Adrenocortical Pathways
  • 6.2.1. Catecholamines
  • TH (Tyrosine Hydroxylase)
  • DR (Dopaminergic receptors)
  • AR (Adrenergic receptors)
  • 6.2.2. Corticoids
  • GC pathway
  • Renin-angiotensin-aldosterone (RAS) system
  • The influence of the RAS system on adipose-tissue physiology:
  • Gender effect on RAS function
  • 6.3. Pancreatic Pathways.
  • 6.3.1. Insulin Signalling Pathway
  • INS (Insulin)
  • INSR (INS receptors)
  • IRS (insulin receptor substrates).
  • 6.4. Adipose Tissue Pathways
  • 6.4.1. Leptin Pathway
  • LEP (Leptin)
  • LEPR (Leptin Receptor)
  • 6.4.2. Adiponectin Pathway
  • 6.4.3. Resistin
  • 6.4.4. Cytokines (TNF, interleukin 6)
  • 6.4.4.1. Interleukin 6
  • IL6 Pathways
  • IL6 Gene
  • 6.4.4.2. Tumor Necrosis Factor-alpha (TNF-α)
  • Pathways
  • Gene
  • IL 6, TNF-α, metabolic syndrome and atherosclerosis
  • 6.4.5. Other Adipokines
  • 6.4.5. PPARs as Key Regulators of the Adipocyte Endocrine Function
  • 6.5. Other Endocrine Pathways
  • 6.5.1. Ghrelin
  • 6.5.2. PYY
  • 7. Gender Differences in Genetic Factors Influencing Metabolic Syndrome Risk
  • 8. Interaction among Elements Influencing Metabolic Syndrome Risk
  • 9. Network of Endocrine Setpoints as a Combined Contributor to Metabolic Syndrome Risk
  • 9.1. Interactions Involving One Single Gene
  • 9.2. Haplotypic Analyses
  • 9.3. Holistic Analysis of Genetic Setpoints
  • [1] References
  • Chapter 2 Reactive Oxygen Species and K+ Channel Function in Diabetes and Insulin Resistance
  • Abstract
  • Introduction
  • Physiological Importance and Basic Structure of K+ Channels
  • KATP Channels
  • Voltage-Gated K+ Channels
  • Ca2+-Activated K+ Channels
  • Impaired Vasomotor Function in Diabetes and Insulin Resistance
  • Hyperglycemia, Oxidative Stress and Sources for Generating Reactive Oxygen Species
  • Activation of Polyol Pathway
  • Activation of Diacylglycerol-Protein Kinase C Pathway
  • Upregulation of NADPH Oxidase
  • Mitochondrial Generation of ROS
  • Hyperglycemia, Reactive Oxygen Species and K+ Channel Function
  • KATP Channels
  • Kv Channels
  • Kca Channels
  • Insulin Resistance and Vascular Disease
  • Insulin Resistance and Vascular Reactivity
  • Insulin Resistance and Potassium Channel Function.
  • Reactive Oxygen Species and Potassium Channel Function in Insulin Resistance
  • Summary and Conclusions
  • References
  • Chapter 3 The Etiology of Obesity-Induced Insulin Resistance
  • Abstract
  • A. Introduction
  • B. Brief Overview of Energy Homeostasis
  • C. Insulin Action
  • C1. Skeletal Muscle
  • C2. Adipose Tissue
  • C3. Liver
  • C4. Vasculature, other
  • D. Insulin-Stimulated Signal Transduction
  • D1. Insulin Receptor
  • D2. Insulin Receptor Substrate
  • D3. Phosphatidylinositol-3-kinase (PI3K)
  • D4. Akt/Protein Kinase B, AS160, and GluT4
  • D5. PI3K-Independent Pathway
  • E. Insulin Resistance and the Metabolic Syndrome
  • F. The Link between Obesity and Insulin Resistance
  • F1. Abdominal Adiposity
  • F1a. Fat Depot Characteristics: VAT vs. SCAT
  • F1b. Counter-arguments for the Pathogenesis of VAT
  • F2. Impaired Glucose Uptake within Fat
  • F3. Glucocorticoids
  • F4. Chronic Inflammation with Obesity
  • F5. The Role of Adipokines in Metabolism, Inflammation, and Insulin Action
  • F5a. Insulin Desensitizing Adipokines: TNF-alpha, IL6, PAI, and Resistin
  • F5ai. TNFα
  • F5aii. IL6
  • F5aiii. PAI-1
  • F5aiv. Resistin
  • F5b. Insulin Sensitizing Adipokines: Leptin and Adiponectin
  • F5bi. Leptin
  • F5bii. Adiponectin
  • F6. Aberrant Lipid Accumulation as an Underlying Cause of Insulin Resistance
  • F6a. Accumulation of Lipids in Lean Tissues
  • F6b. Mechanisms of Lipid-Induced Insulin Resistance
  • F6bi. Diacylglycerol
  • F6bii. Ceramides
  • F7. ER Stress
  • F8. Oxidative Stress and Reactive Oxygen Species
  • G. Perspective on Insulin Resistance and Treatment
  • H. Selected References
  • Chapter 4 Racial/Ethnic Disparities in Hypertension and Diabetes Ascribed to Differences in Obesity rate
  • Abstract
  • Context
  • Objective
  • Methods
  • Results
  • Conclusion
  • Introduction
  • Racial/Ethnic Differences in Hypertension.
  • Racial/Ethnic Differences in Type 2 Diabetes
  • Racial/Ethnic Differences in Obesity
  • Explanatory Power of Obesity for Racial/Ethnic Variations in Hypertension and Diabetes
  • Methodologic Issues Associated with Studying Obesity and Racial/Ethnic Variations in Diseases
  • Obesity Measurement
  • Quantifying Obesity Risk
  • Estimation of Odds Ratio
  • Estimation of Relative Risk
  • Quantifying Obesity Impact
  • Population Attributable Risk
  • Relative Attributable Risk
  • Objective of Study
  • Methods
  • Definition of Terms
  • Statistical Analysis
  • Results
  • Discussion
  • Public Health Implications of Findings
  • Conclusion
  • References
  • Chapter 5 Chosen Life Aspects of Diabetic Patients
  • Abstract
  • Diabetic Patient on a Journey
  • Medical Dilemmas on Eligibility for Driving Licenses
  • Access to Education and Employment for Diabetic Patient
  • Problems with Education of Young Diabetic Patients
  • Employment of Diabetic Patients
  • Insurance
  • References
  • Chapter 6 CNS Amyloidosis and Diabetes Mellitus: Vicious Circles of Misfolding
  • Abstract
  • Conclusion
  • References
  • Chapter 7 Erythrocyte Transplasma Membrane Electron Transport, Oxidative Stress, Body Mass and Lifestyle in Healthy and in Type 1 Diabetic Families
  • Abstract
  • Abbreviations
  • Degenerative Diseases and Redox Cycling
  • Transplasma Membrane Electron Transport Systems
  • Electron Transfer across the Red Cell Membrane
  • Diet, Lifestyle and Cell Antioxidant Capacity
  • Our Previous Observations
  • Objectives of the Study
  • Method
  • Result
  • Conclusion
  • Acknowledgments
  • References
  • Chapter 8 Impact of Oxidative Stress on Diabetes Mellitus and Inflammatory Bowel Diseases
  • Abstract
  • 2. Introduction
  • 2.1 ROS under Physiological Conditions
  • 2.2 ROS under Pathological Conditions
  • 2.3 Antioxidant Defence of Human Organism.
  • 2.4 Some Remarks to Antioxidant Enzymes and Substances from the Recent Literature
  • 2.5 Non-enzymatic Substances of Endogenous or Exogenous Origin
  • Thioredoxin (Trx)
  • Coenzyme Q10 (CoQ)
  • Vitamin C
  • Vitamin E
  • Phytochemicals
  • 2.6 Catalytic Antioxidants
  • New Therapeutic Possibilities
  • 3. DNA Oxidative Damage and DNA Repair
  • Nuclear DNA Damage and Repair
  • MItochondrial DNA Damage and Repair
  • 3.3 Poly(ADP-ribose) Polymerase
  • 3.4 Diseases Related with Oxidative Stress and DNA Damage
  • 4. Oxidative Stress and Pathophysiology of Diabetes Mellitus and Inflammatory Bowel Diseases
  • 4.1 Diabetes Mellitus
  • 4.1.1 ROS and Diabetes
  • ROS, DNA Damage and DM
  • ROS, DNA Repair and DM
  • Some Contributions to Antioxidant Therapy in Diabetes Mellitus
  • 4.2 Crohn´s Disease
  • ROS and IBD
  • ROS, DNA Damage, DNA Repair and IBD
  • 5. Our Study Examining Oxidative Stress, DNA Damage and DNA Repair in Patients with Diabetes Mellitus and Crohn Disease
  • 5.1 Hypothesis
  • 5.2 Study Material
  • 5.3 Methods
  • 5.4 Results
  • 5.4.1 Study of Oxidative Stress, DNA Damage and DNA Repair Capacity of Lymphocytes in Healthy Adults and Healthy Children
  • 5.4.2 Comparison of T1DM Patients versus Healthy Population
  • 5.4.3 Comparison of T1DM Adult Group versus T1DM Children
  • 5.4.4 Comparison of T1DM Adults Divided into 2 Subgroups Based on the Abscence or Presence of Diabetic Microvascular Complications with T1DM Children (Published by Varvarovska, Biomedicine and Pharmacotherapy 2004, Citation 136)
  • 5.4.5 Study of CD Patients (Adults and Children) versus Healthy Adult Population
  • 5.4.6 Comparison of Adult CD Patients with CD Children
  • 5.4.7 Comparison of Adult Diabetic Patients and Patients with Crohn's Disease
  • 5.4.8 Children with T1DM and CD Compared with Healthy Children
  • 5.4.9 Comparison between T1DM and CD Children.

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