Obesity, diabetes and inflammation : molecular mechanisms and clinical management / Dimiter Avtanski, Leonid Poretsky, editors.
Obesity is a worldwide epidemic that affects half a billion people. It has been estimated that, if current trends continue, by 2050, 60% of men and 50% of women worldwide will be obese. Hypertrophy and hyperplasia of white adipose tissue caused by overweight and obesity lead to a chronic inflammator...
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Full Text (via Springer) |
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| Other Authors: | , |
| Format: | Electronic eBook |
| Language: | English |
| Published: |
Cham :
Springer,
2023.
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| Series: | Contemporary endocrinology (Totowa, N.J.)
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Table of Contents:
- Intro
- Preface
- Contents
- Chapter 1: Inflammation: Pathogenesis and Biological Markers
- Introduction
- Brief History and Definitions
- Clinical Biomarkers
- Immunology of Inflammation
- Innate Immune System
- Cells of the Innate Immune System
- Molecular Components of the Innate Immune System
- Adaptive Immune System
- Components of Adaptive Immunity
- Chronic Inflammation Associated with Adaptive Immunity
- Anti-Inflammatory Therapy
- Conclusions
- References
- Chapter 2: Obesity and Inflammation
- Introduction
- Obesity
- Adipose Tissue
- Introduction
- Epidemiology and Risk Factors
- Genetics
- Inflammation, the Immune System, and Diabetes
- The Role of Cytokines in the Development of Diabetes
- Immune Checkpoint Inhibitor-Induced Diabetes
- Treatment
- Metformin
- Glucagon-Like Peptide-1 (GLP-1) Receptor Agonists
- Sodium-Glucose Co-Transporter 2 Inhibitors
- Immune-Based Therapies
- Systemic Inflammation and Diabetes
- Conclusions
- References
- Chapter 4: Diabetes, Obesity, and Oxidative Stress
- Introduction
- Oxidative Stress
- Obesity, Diabetes and Insulin Resistance
- Key Molecular Mechanisms of Obesity, IR and DM Include Mitochondrial Dysfunction, ER Stress and ROS-Induced DNA Damage, which Are Closely Connected with the Major Cellular Disturbances Caused by OS
- Mitochondrial Dysfunction
- Endoplasmic Reticulum Stress
- ROS-Induced DNA Damage
- Conclusions
- References
- Chapter 5: Advanced Glycation End Products and Diabetes
- Advanced Glycation End Products: Sources, Metabolism, Interaction with Receptors
- Exogenous AGEs
- Endogenous AGEs
- Metabolism of AGEs
- Interaction of AGEs with Receptors
- AGEs in Type 2 Diabetes Mellitus: Pathophysiological Mechanisms
- AGEs Are Toxic to β-Cells and Negatively Influence Insulin Production and Secretion
- AGE-Induced Insulin Resistance
- AGEs and Chronic Diabetic Complications
- AGEs in Diabetic Cardiovascular Diseases
- AGEs in Diabetic Kidney Disease
- Therapeutic Options to Reduce AGEs in Diabetes
- Dietary Intervention
- Neutralization and Signaling Interference
- Pharmacological Agents
- Nutritional and Phytotherapeutic Options
- References
- Chapter 6: Genetic and Epigenetic Basis of Obesity-Induced Inflammation and Diabetes
- White Adipose Tissue and Obesity
- Brown Adipose Tissue and Obesity
- Obesity and Inflammation
- Overview
- Cytokines Involved in Obesity-Induced Inflammation
- Leptin
- Adiponectin
- Resistin
- TNFα
- IL-6
- Irisin
- Inducers of Adipose Tissue Inflammation in Obesity
- ER Stress
- Imbalance in Fatty Acids Homeostasis
- Hypoxia
- Mitochondrial Dysfunction
- Adipose Tissue Inflammation and Immune System Cells
- Macrophages
- Neutrophils
- Dendritic Cells
- Mast Cells
- B Cells
- T Cells
- Conclusions
- References
- Chapter 3: Inflammation and Diabetes Mellitus