Diabetes Mellitus Research Advances.

By: Huber, Maximilian N
Publisher: Hauppauge : Nova Science Publishers, Incorporated, 2008Copyright date: ©2009Description: 1 online resource (345 pages)Content type: text Media type: computer Carrier type: online resourceISBN: 9781608766031Subject(s): DiabetesGenre/Form: Electronic books. Additional physical formats: Print version:: Diabetes Mellitus Research AdvancesDDC classification: 616.462 LOC classification: RC660 -- .D5419 2008ebOnline resources: Click to View
Contents:
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.
5.4.10 Comparison of all Groups of Patients versus Healthy Adults.
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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.

5.4.10 Comparison of all Groups of Patients versus Healthy Adults.

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