| 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 | |
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