Controversies In Diabetic Neuropathy

 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 28. April 2016
  • |
  • 392 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
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978-0-12-803940-3 (ISBN)
 

This latest volume in the International Review of Neurobiology series, provides a comprehensive overview of the state-of-the-art research on the topic. It reviews the current knowledge and understanding in the field, presenting a starting point for researchers and practitioners entering the field.


  • Offers a comprehensive overview of state-of-the-art research on diabetic neuropathy
  • Provides personal critiques from experts in each field
  • Provides a running commentary by editors throughout the book
  • Explores a range of topics including mechanisms of nerve damage, neuropathic pain, new therapies, clinical trials, and animal models of diabetic neuropathy
0074-7742
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 15,65 MB
978-0-12-803940-3 (9780128039403)
012803940X (012803940X)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Controversies In Diabetic Neuropathy
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Section I: Clinical Context
  • Chapter One: A Brief Introduction to the History and Controversies of Clinical Trials in Diabetic Neuropathy
  • References
  • Chapter Two: Neuropathy in the DCCT/EDIC-What Was Done Then and What We Would Do Better Now
  • 1. Introduction
  • 2. Neuropathy Outcomes Assessments
  • 2.1. DCCT and EDIC Design
  • 2.1.1. Assessment of DSPN in DCCT
  • 2.1.2. Assessment of DSPN in EDIC
  • 2.1.3. Additional DSPN Measures in EDIC
  • 2.1.4. Assessment of CAN in DCCT
  • 2.1.5. Assessment of CAN in EDIC
  • 3. Complementary Assessments in EDIC
  • 3.1. Evaluation of Urologic Complications
  • 3.2. Gastroparesis
  • 3.3. Other Evaluations in EDIC
  • 4. DCCT/EDIC Findings
  • 4.1. DSPN and CAN Outcomes in the DCCT and EDIC Study
  • 5. Discussion
  • 5.1. DCCT/EDIC and Contemporary Neuropathy Trials Design
  • References
  • Chapter Three: The Perfect Clinical Trial
  • 1. Introduction
  • 2. Study Aims: Prevent DSP, Prevent Progression, or Reverse DSP?
  • 3. Selection of Study Participants
  • 4. Trial Duration
  • 5. Study End Points
  • 6. Core Labs and Training
  • 7. Intervention
  • 8. Study Conduct
  • 9. Streamlined Ethics and Contracts Process
  • 10. Summary
  • References
  • Section II: New Models of Diabetic Neuropathy
  • Chapter Four: An Introduction to the History and Controversies of Animal Models of Diabetic Neuropathy
  • 1. Why Use Animal Models?
  • 2. What Species?
  • 3. What Diabetogenic Insult?
  • 4. STZ Toxicity
  • 5. Novel Models
  • References
  • Chapter Five: Can Diabetic Neuropathy Be Modeled In Vitro?
  • 1. Introduction
  • 2. Diabetic Neuropathy
  • 3. The Somatosensory Nervous System
  • 4. Can We Model Diabetic Neuropathy In Vitro?
  • 4.1. Choice of Cells
  • 4.1.1. Immortalized Cell Lines
  • 4.1.2. Primary Tissue Culture
  • 4.1.3. Induced Pluripotent Stem Cells
  • 4.2. Choice of Stimuli
  • 4.3. Choice of Output Measure
  • 4.3.1. Life or Death?
  • 4.3.2. Altered Bioenergetics and Oxidative Stress
  • 4.3.3. Neuronal Hyperexcitability
  • 4.3.4. Axonal Degeneration and Regeneration
  • 4.4. Looking Forward to a Better In Vitro Model of Diabetic Neuropathy
  • 5. Conclusions
  • Acknowledgments
  • References
  • Chapter Six: Alternatives to the Streptozotocin-Diabetic Rodent
  • 1. Introduction
  • 2. Rodent Models of Obesity
  • 2.1. High-Fat Fed Sprague-Dawley Rats and C57Bl6/J Mice
  • 2.2. Zucker Rats
  • 3. Rodent Models of Type 2 Diabetes
  • 3.1. Zucker Diabetic Fatty Rats
  • 3.2. Spontaneously Diabetic Torii Rat
  • 3.3. Zucker Diabetic Sprague-Dawley Rat
  • 3.4. Goto-Kakizaki Rat
  • 3.5. BioBreeding Zucker Diabetic Rat
  • 3.6. Otsuka Long-Evans Tokushima Fatty Rat
  • 3.7. Ob/ob and db/db Mice
  • 3.8. Tsumura Suzuki Obese Diabetes Mouse
  • 3.9. Combined High-Fat Fed, Low-Dose Streptozotocin Models of Type 2 Diabetes
  • 3.10. Streptozotocin-Nicotinamide Rat
  • 4. Rodent Models of Type 1 Diabetes
  • 4.1. Spontaneously Hypertensive Rat
  • 4.2. BioBreeding/Worcester Rat
  • 4.3. Ins2Akita Mouse
  • 4.4. Nonobese Diabetic Mouse
  • 5. Other Animal Models
  • 6. Conclusions
  • References
  • Section III: Mechanisms and Therapies
  • Chapter Seven: An Introduction to the History and Controversies of the Pathogenesis of Diabetic Neuropathy
  • References
  • Chapter Eight: Glucotoxic Mechanisms and Related Therapeutic Approaches
  • 1. Introduction
  • 2. Glucose-Metabolizing Pathways Relevant to DPN
  • 3. Polyol (AR or Sorbitol-Fructose) Pathway
  • 3.1. Metabolic Sequelae After Increased Flux Through the Polyol Pathway
  • 3.2. Studies in Transgenic and Knockout Mice
  • 3.3. Effects of AR Inhibition
  • 3.4. Clinical Application of ARIs
  • 3.5. Polyol Pathway in Ischemia/Reperfusion Injury
  • 4. Nonenzymatic Glycation and AGEs
  • 4.1. Glycation of Proteins in Diabetes
  • 4.2. Glycation and AGE in DPN
  • 4.3. Transgenic and Knockout Mice Studies
  • 4.4. Clinical Application of Antiglycation Agents
  • 5. Oxidative Stress
  • 5.1. Production of Oxidative Stress by Hyperglycemia
  • 5.2. Oxidative Stress and Diabetic Neuropathy
  • 5.3. Effects of Antioxidants on Diabetic Neuropathy
  • 6. PKC Activity
  • 7. Glycosylation
  • 7.1. The Hexosamine Pathway
  • 7.2. Other Glycosylation Events
  • 8. Conclusion
  • Acknowledgments
  • References
  • Chapter Nine: Sensory Neurodegeneration in Diabetes: Beyond Glucotoxicity
  • 1. Terminals at Risk: Sensory Neurodegeneration in Diabetes
  • 2. Not Necessarily a Microvascular Disease
  • 3. Altered Insulin Signaling
  • 4. Ongoing Growth: Other Forms of Support
  • 4.1. C-Peptide
  • 4.2. Glucagon-Like Peptide-1
  • 4.3. Heat-Shock Proteins
  • 5. Neurons "on Edge"
  • 6. Diabetes, Neurons, and Epigenetics
  • 7. A Regeneration Strategy
  • 8. Conclusions
  • Acknowledgments
  • References
  • Chapter Ten: Promoting Neuronal Tolerance of Diabetic Stress: Modulating Molecular Chaperones
  • 1. Introduction
  • 2. Molecular Chaperones
  • 3. Extracellular Hsp70
  • 3.1. Import, Export, and Neuronal Support
  • 3.2. Immunomodulation, Inflammation, and Oxidative Stress
  • 4. Intracellular Hsp70
  • 4.1. Chaperone Functions
  • 4.2. Oxidative Stress
  • 4.3. Inflammation
  • 4.4. Insulin Sensitivity, JNK, and c-Jun
  • 5. DPN and Modulating Hsp70
  • 6. Concluding Remarks
  • Acknowledgments
  • References
  • Chapter Eleven: Painful Diabetic Neuropathy: Prevention or Suppression?
  • 1. Introduction
  • 2. Nociceptive Ion Channels Control Neuronal Excitability
  • 3. Alterations of Voltage-Gated and Ligand-Gated Ion Channels in Sensory Neurons in Animal Models of Type 1 Diabetes
  • 4. Alterations of CaV3.2 T-Type Channels in Nociceptive Sensory Neurons in Animal Models of Type 2 Diabetes with Painful PDN
  • 5. Posttranslational Modification of Pronociceptive Ion Channels in PDN
  • 6. Diminished Inhibitory Drive in the Spinal Cord May Also Contribute to Painful PDN
  • 7. Conclusions
  • Acknowledgments
  • References
  • Section IV: Translating Science into Medicine
  • Chapter Twelve: New Directions in Diabetic Neuropathy: Evolution or Extinction?
  • 1. NCV as an Endpoint in Animal Models
  • 2. Treatment Paradigms
  • 3. Insanity: Doing the Same Thing Over and Over Again and Expecting a Different Result
  • References
  • Chapter Thirteen: Alternative Quantitative Tools in the Assessment of Diabetic Peripheral and Autonomic Neuropathy
  • 1. Introduction
  • 2. Diabetic Peripheral Neuropathy
  • 2.1. Clinical Presentation
  • 2.2. Diagnosis
  • 2.3. Falls Risk in Older Adults with Diabetes
  • 2.3.1. Falls and Aging
  • 2.3.2. Risk of Falling Is Increased for Older Adults with Type 2 Diabetes
  • 2.3.3. Neuropathy Is Strongly Linked to Falling
  • 2.3.4. Can Risk of Falling Be Reversed?
  • 3. Diabetic Autonomic Neuropathy
  • 3.1. Clinical Manifestations
  • 3.2. Cardiovascular Autonomic Neuropathy
  • 3.2.1. Diagnosis of CAN
  • 3.2.2. Cardiovascular Symptoms and Signs
  • 3.2.2.1. Resting Tachycardia
  • 3.2.2.2. Exercise Intolerance
  • 3.2.2.3. Intraoperative Cardiovascular Liability
  • 3.2.2.4. Orthostatic Hypotension
  • 3.2.2.5. Silent Myocardial Ischemia/Cardiac Denervation Syndrome
  • 3.2.2.6. Increased Risk of Mortality
  • 3.2.2.7. Increased Mortality After MI
  • 3.2.2.8. CAN and Sudden Death
  • 3.2.3. Impact of CAN on Diabetes Management
  • 3.3. Prevention and Reversibility of Autonomic Neuropathy
  • 4. Measuring Diabetic Neuropathy: Established and Innovative Approaches
  • 4.1. QOL Measures
  • 4.2. Clinical Assessment Tools
  • 4.3. Objective Measurements
  • 4.3.1. Nerve Conduction Studies
  • 4.3.2. Skin Biopsy
  • 4.3.3. Corneal Confocal Microscopy
  • 4.3.4. Contact Heat Evoked Potentials
  • 4.3.5. LDI Flare
  • 4.3.6. Assessment of Autonomic Neuropathy
  • 4.3.7. Sudorimetry
  • 4.3.7.1. Clinical Diagnostic Evaluation Using Sudomotor Function
  • 4.3.7.2. Validation of ESC Robustness
  • 4.3.7.3. Sudomotor Function as a Tool to Measure Progression and Regression of Disease
  • 5. Concluding Remarks
  • References
  • Chapter Fourteen: Wherefore Art Thou, O Treatment for Diabetic Neuropathy?
  • 1. The Problem
  • 2. What Can We Do?
  • 3. Diagnostic Tests are Not Necessarily Good Surrogate End Points
  • 4. Clinical Trials in Diabetic Neuropathy
  • 4.1. Glycemic Control
  • 4.2. Pancreas Transplantation
  • 4.3. a-Lipoic Acid
  • 4.4. Aldose Reductase Inhibitors
  • 4.5. Vitamin B
  • 4.6. Angiotensin-Converting Enzyme Inhibitors
  • 4.7. Protein Kinase C Activation
  • 4.8. C-Peptide
  • 4.9. Actovegin
  • 4.10. Disease Modification
  • 4.11. Nerve Growth Factor
  • 4.12. Other Growth Factors
  • 4.13. Erythropoietin
  • 4.14. Vitamin D
  • 4.15. Angiotensin Axis
  • 5. Can We Ever Succeed?
  • References
  • Index
  • Contents of Recent Volumes
  • Back Cover

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