Diabetes mellitus research advances / Maximilian N. Huber, editor.

Format:

Book

Contributor:

Huber, Maximilian N.

Language:

English

Subjects (All):

Diabetes.

Physical Description:

1 online resource (345 p.)

Edition:

1st ed.

Place of Publication:

New York : Nova Science Publishers, 2008.

Language Note:

English

Summary:

Diabetes mellitus is a chronic disease of absolute or relative insulin deficiency or resistance characterized by disturbances in carbohydrate, protein and fat metabolism. It is estimated that between 5-10% of the population suffer from this disease. This syndrome is a contributing factor in a large percentage of deaths from heart attacks and strokes as well as renal failure and vascular disease. About 90% of the cases of diabetes mellitus fall into Type 2 where obesity plays a major role. Research in the field is wide-spread ranging from causes to treatment. This new book presents the lastest research in the field.

Contents:

Intro

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

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

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

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

Context

Objective

Methods

Results

Conclusion

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

Definition of Terms

Statistical Analysis

Discussion

Public Health Implications of Findings

Chapter 5 Chosen Life Aspects of Diabetic Patients

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

Chapter 6 CNS Amyloidosis and Diabetes Mellitus: Vicious Circles of Misfolding

Chapter 7 Erythrocyte Transplasma Membrane Electron Transport, Oxidative Stress, Body Mass and Lifestyle in Healthy and in Type 1 Diabetic Families

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

Acknowledgments

Chapter 8 Impact of Oxidative Stress on Diabetes Mellitus and Inflammatory Bowel Diseases

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.

Notes:

Description based upon print version of record.

Includes bibliographical references and index.

Description based on print version record.

ISBN:

1-60876-603-9

OCLC:

923668155