Aetiology of Insulin Resistance and Type 2 Diabetes: Prevalence and Consequences of the "Diabesity" Epidemic | |
The Increasing Burden of Type 2 Diabetes: Magnitude, Causes, and Implications of the Epidemic | |
Trends in Prevalence and Incidence | |
Risk Factors for Diabetes and Causes of the Epidemic | |
Determinants of Recent Trends in the Epidemic | |
Anticipated Consequences of Diabetes and the Outlook for Prevention | |
Concluding Remarks | |
Waging War on Type 2 Diabetes: Primary Prevention Through Exercise Biology | |
Scope of the Problem | |
Rationale for action | |
Physical Inactivity's Contributing Role in the Pathogenesis of Diabetes | |
New Ammunitions | |
Future Battle Plans | |
Concluding Remarks | |
Defects in Metabolism and Insulin Resistance | |
Fatty Acid Uptake and Insulin Resistance | |
LCFAS and Their Uptake Across the Sarcolemma | |
Fatty Acid Transporters | |
Fatty Acid Transport and Transporters in Human Obesity and Type 2 Diabetes | |
Concluding Remarks | |
Lipid Metabolism and Insulin Signaling | |
Lipid Metabolism in Skeletal Muscle | |
The Insulin-Signaling Pathway | |
Does Lipid Exposure Impair Insulin Action? | |
Perturbations in Lipid Metabolism, Insulin Signal Transduction, and Insulin Action With Type 2 Diabetes and Obesity | |
The Exercise Paradox | |
Effect of Weight Loss on Muscle Lipid Accumulation and Insulin Signaling | |
Concluding Remarks | |
Metabolic Inflexibility and Insulin Resistance | |
Substrate Utilization During Resting Conditions in Lean, Healthy Individuals | |
Substrate Utilization in Insulin-Resistant Individuals | |
Potential Cellular Mechanisms for Metabolic Flexibility in Fat Oxidation | |
Effects of Weight Loss on Metabolic Flexibility in Obesity and T2DM | |
Effects of Exercise Training on Metabolic Flexibility in Obesity and T2DM | |
Concluding Remarks | |
Nutrient Sensor Links Obesity With Diabetes Risk | |
Nutrient Sensing and Control of Food Intake | |
Overnutrition, Disruption of Homeostatic Control, and Insulin Resistance | |
Cellular Nutrient Sensing | |
Concluding Remarks | |
Inflammation-Induced Insulin Resistance in Obesity: When Immunity Affects Metabolic Control | |
Obesity Is a Chronic Low-Grade Inflammatory State | |
Evolution of Inflammation in Obesity | |
Lipid Mediators | |
Protein Kinase Mediators | |
Transcriptional Mediators | |
Concluding Remarks | |
Prevention of Type 2 Diabetes Through Exercise Training | |
Transcription Factors Regulating Exercise Adaptation | |
Activation of MAP Kinase Signaling | |
Factor of Activated T Cells (NFAT) | |
Regulation of GLUT4 Expression | |
Mitochondria Biogenesis and Increased Lipid Oxidation | |
Exercise-Mediated Regulation of PPARs | |
Peroxisome Proliferators Activated Receptor Gamma Coactivator (PGC)-1 | |
Concluding Remarks | |
Exercise and Calorie Restriction Use Different Mechanisms to Improve Insulin Sensitivity | |
Exercise and Calorie Restriction Effects on Skeletal Muscle Energy Status | |
Exercise/Contraction-Stimulated Signaling Pathway for Glucose Transport | |
Exercise Training Effects on Insulin Sensitivity and Insulin Signaling | |
Effects of Calorie Restriction Distinct From Weight Loss | |
Effects of Calorie Restriction on Insulin Signaling in Skeletal Muscle | |
Combined Effects of Exercise and Calorie Restriction | |
Concluding Remarks | |
Mitochondrial Oxidative Capacity and Insulin Resistance | |
An Overview of Mitochondrial Structure and Function | |
Evidence for a Role for Mitochondria in Insulin Resistance and Diabetes | |
Evidence That Mitochondria Are Not Responsible for Insulin Resistance | |
Concluding Remarks | |
Effects of Acute Exercise and Exercise Training on Insulin Action in Skeletal Muscle | |
Exercise and Contraction Signaling in Muscle | |
Insulin Signaling: A Web | |
Effect of a Single Bout of Exercise on Insulin Sensitivity | |
Effects of Exercise Training on Insulin Action | |
Concluding Remarks | |
Resistance Exercise Training and the Management of Diabetes | |
Resistance Training and Insulin Sensitivity | |
Mechanisms Behind Resistance Training-Induced Improvements in Insulin Sensitivity | |
Training-Induced Gene Expression | |
Conclusion and Perspectives | |
Concluding Remarks | |
Prevention of Type 2 Diabetes: Identification of Novel Molecular Targets and Pathways | |
AMPK: The Master Switch for Type 2 Diabetes? | |
Discoveries Suggesting AMPK Could Be Important for Prevention and Treatment of Type 2 Diabetes | |
Could Type 2 Diabetes Be a Consequence of Deficiency in AMPK Signaling? | |
How Can AMPK Activation Help Prevent Type 2 Diabetes? | |
Can Chemical AMPK Activation Prevent Diabetes? | |
Feasibility of Using AMPK Activators | |
Future Directions | |
Concluding Remarks | |
Protein Kinase C and Insulin Resistance | |
The PKC Family of Serine or Threonine Kinases | |
Roles for PKC in Normal Glucose Homeostasis | |
PKC and Defective Glucose Disposal | |
Concluding Remarks | |
Evidence for the Prescription of Exercise as a Therapy for the Treatment of Patients With Type 2 Diabetes | |
Options for the Treatment of Insulin Resistance and Type 2 Diabetes | |
Molecular Evidence for the Prescription of Exercise Training | |
Exercise and Drug Combination Therapy | |
Exercise-Like Effects of Current Antihyperglycemic Drugs | |
Prescription of Exercise Training: Practical Considerations | |
Concluding Remarks | |
Table of Contents provided by Publisher. All Rights Reserved. |