Umfang:
Online-Ressource (XIII, 433 p. 37 illus., 28 illus. in color, digital)
ISBN:
9781461468196
Serie:
Energy Balance and Cancer 7
Inhalt:
In addition to their metabolic and endocrinologic effects, obesity and adipose tissue have now been shown to be associated with chronic low grade inflammation resulting in cellular and humoral factors of which the latter may act by endocrine, paracrine and autocrine mechanisms. These inflammatory mediators have increasingly been suggested as contributing to the obesity link to carcinogenesis and cancer promotion. Obesity, Inflammation and Cancer focuses on recent developments and cutting edge research pointing to inflammation and inflammatory factors as key mediators of this linkage. It also describes possible strategies for targeting inflammation as an approach to cancer prevention and control. Students, researchers and clinicians, especially those interested in the relation of obesity to cancer and the role of inflammation and its impact on cancer, will find this volume particularly useful. It provides important insight on the role of inflammation in cancer etiology and progression and serve as a platform for developing future research in this area
Anmerkung:
Includes bibliographical references and index
,
Preface: What's Old Is New Again and Now It's Red Hot; Contents; Contributors; Chapter 1: Obesity, Inflammation, and Insulin Resistance; 1.1 Introduction; 1.2 Insulin Signaling; 1.3 Immune Cells; 1.3.1 Macrophages; 1.3.2 Neutrophils; 1.3.3 CD4 + T Cells: T-Helper and T-Regulatory Cell Subsets; 1.3.4 CD8 + T Cells; 1.3.5 B Cells; 1.3.6 Natural Killer T Cells; 1.3.7 Eosinophils; 1.3.8 Mast Cells; 1.4 Signaling Pathways Linking Inflammation and Insulin Resistance; 1.4.1 Cytokine Signaling; 1.4.2 Lipid Signaling; 1.4.3 ER Stress; 1.4.4 Hypoxia; 1.5 Anti-inflammatory Therapies
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1.6 Links with Cancer1.7 Conclusions; References; Chapter 2: Inflammasomes and Obesity; 2.1 Inflammasomes Are Key Mediators of the Innate Immune System; 2.2 The NLRP3 Inflammasome is a Major Mediator of Human Disease; 2.2.1 NLRP3 Inflammasome-Priming Signals; 2.2.2 The Assembly of the NLRP3 Inflammasome; 2.3 The Diverse Regulation of NLRP3 Inflammasome Activation; 2.3.1 Reactive Oxygen Species; 2.3.2 Cytoplasmic Potassium; 2.3.3 Phagocytosis and Lysosomal Damage; 2.3.4 The NLRP3 Inflammasome is Negatively Regulated by IFNγ and T Cell Responses; 2.4 NLRP3 Inflammasome Is a Metabolic Regulator
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2.4.1 Fatty Acids2.4.2 Hyperglycemia; 2.4.3 Uric Acid and MSU Crystals; 2.4.4 Cholesterol; 2.4.5 Amyloid; 2.5 Obesity and the NLRP3 Inflammasome; 2.5.1 Chronic Inflammation in Adipose Tissue; 2.5.2 NLRP3 Inflammasome Expression and Activity in Obese Mice; 2.5.3 NLRP3 Inflammasome Expression and Activity in Obese Patients; 2.5.4 Mechanisms of NLRP3 Inflammasome Activation in Adipose Tissue; 2.6 The NLRP3 Inflammasome in Metabolic Diseases Associated with Obesity; 2.6.1 Type 1 and Type 2 Diabetes; 2.6.2 Metabolic Liver Disease; 2.6.3 Atherosclerosis; 2.6.4 Gout; 2.6.5 Alzheimer's Disease
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2.7 Cancer, Obesity and Inflammation2.7.1 Cell Death and Inflammasome Activity; 2.7.2 The Inflammasomes and Carcinogenesis; 2.7.3 Inflammasome-Dependent Anticancer Responses; 2.8 Pharmaceutical Interventions Targeting the Inflammasome; 2.8.1 Therapeutics Targeting IL-1β Activity; 2.8.2 Therapeutic Approaches Acting on the Inflammasome or Caspase-1; 2.8.3 Other Therapeutic Targets to Attenuate Inflammasome Activity; 2.9 Summary; References; Chapter 3: Uncoupling Obesity from Cancer: Bromodomain Co-regulators That Control Inflammatory Networks; 3.1 The Problem of Obesity-Associated Cancer
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3.2 Molecular Features of Insulin-Resistant Obesity3.3 Insulin-Resistant Obesity Is Also an Inflammatory Disease; 3.4 Insight from Unexpected Results; 3.5 Other Links Between Obesity, Inflammation, and Social Determinants; 3.6 Interactions Among Biological and Social Factors; References; Chapter 4: Adipose Tissue Macrophages in Obesity, Inflammation, and Cancer; 4.1 Introduction; 4.2 Adipose Tissue Macrophages as Inflammatory Engines in Obesity; 4.3 Adipose Tissue Macrophage Diversity; 4.3.1 Macrophage Activation States; 4.3.2 The M1/M2 Paradigm in Obesity
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4.3.3 The Nature of the Phenotypic Shift from M2-Like to M1-Like ATMs in Obesity
Weitere Ausg.:
ISBN 9781461468189
Weitere Ausg.:
Erscheint auch als Druck-Ausgabe Obesity, inflammation and cancer New York, NY : Springer, 2013 ISBN 9781461468189
Sprache:
Englisch
Fachgebiete:
Medizin
Schlagwort(e):
Fettsucht
;
Entzündung
;
Carcinogenese
DOI:
10.1007/978-1-4614-6819-6
URL:
Volltext
(lizenzpflichtig)
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