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G protein-coupled receptors in energy homeostasis and obesity pathogenesis
1 online resource (xiii, 387 pages) : illustrations (some color)
Obesity is an epidemic with enormous health, economic and social burdens. Current drugs for obesity treatment are far from ideal in terms of efficacy and side effects. Reviews in this volume of Progress in Molecular Biology and Translational Science summarize current status in studies of a number of G protein-coupled receptors that were shown to be promising targets for obesity treatments. Some of these receptors also cause monogenic obesity in humans. Subject matter: obesity is an epidemic and G protein-coupled receptors are promising drug targets, with significant potential as new anti-obesity drugs. Chapters are written by leading experts.
Front Cover ; G Protein-Coupled Receptors in Energy Homeostasis and Obesity Pathogenesis; Copyright; Contents; Contributors; Preface; Chapter One: G Protein-Coupled Receptors as Regulators of Energy Homeostasis; 1. Introduction to G Protein-Coupled Receptors; 2. Obesity and Current Treatments; 3. Regulation of Energy Homeostasis in the Central Nervous System; 4. Regulation of Energy Homeostasis by the GI Peptides; 5. Regulation of Energy Homeostasis by Peptides from Endocrine Pancreas; 6. Regulation of Energy Homeostasis by Orphan GPCRs.
7. Regulation of Energy Homeostasis by GPCRs in Domestic Animals8. Regulation of Energy Homeostasis by GPCRs in Lower Vertebrates; 9. Genetics of Human Obesity; 10. Summary; Acknowledgments; References; Chapter Two: Ghrelin Receptor in Energy Homeostasis and Obesity Pathogenesis; 1. Overview of the Ghrelin Receptor; 1.1. Discovery of the ghrelin receptor; 1.1.1. Development of growth hormone secretagogue; 1.1.2. Identification of GHS-R; 1.2. Natural ligands for the ghrelin receptor; 1.3. Variants of the ghrelin receptor; 1.4. Antagonists for the ghrelin receptor.
1.5. Structure of ghrelin receptor and ligand-binding domains1.6. Constitutive activity of ghrelin receptor; 1.7. Internalization of ghrelin receptor; 1.8. Interaction between the ghrelin receptor and other receptors; 1.8.1. The ghrelin receptor and the GHRH receptor; 1.8.2. Ghrelin receptor and dopamine receptors; 1.8.2.1. Ghrelin receptor and D1-R (dopamine receptor subtype-1); 1.8.2.2. The ghrelin receptor and D2-R (dopamine receptor subtype-2); 1.8.3. The ghrelin receptor and melanocortin-3 receptor; 1.8.4. The ghrelin receptor and the adenosine receptor.
1.9. Intracellular signaling pathways1.9.1. Calcium mobilization-related signaling; 1.9.2. MAPK signaling; 1.9.3. AMPK signaling; 1.9.4. PI3K/AKT signaling; 1.10. Distribution of the ghrelin receptor; 1.11. Life without the ghrelin receptor; 1.11.1. Condition of normal chow diet; 1.11.2. Condition of high-fat diet; 1.11.3. Aging-associated obesity; 2. The Ghrelin Receptor and Energy Metabolism; 2.1. Regulation of food intake; 2.2. Glucose homeostasis; 2.2.1. Effect of exogenous ghrelin; 2.2.2. Effect of endogenous ghrelin; 2.2.3. Response altered by energy status.
2.2.4. Effects on the major target organs for insulin2.2.4.1. Pancreas; 2.2.4.1.1. Effect on the development of Ý-cells; 2.2.4.1.2. Effect on insulin secretion; 2.2.4.2. Skeletal muscle; 2.2.4.3. Liver; 2.2.4.4. Adipocytes; 2.3. Lipid metabolism; 2.3.1. Central effect; 2.3.2. Peripheral effect; 2.4. Ghrelin receptor polymorphism and energy metabolism; 3. Strategies for Treatment of Obesity and Diabetes; 3.1. Ghrelin receptor antagonists?; 3.2. Alteration of ghrelin sensitivity in obesity and diabetes?; 3.3. Targeting the brain or the stomach, a lesson from gastric bypass surgery?
Includes bibliographical references and index.
Amsterdam ; Boston : Elsevier/Academic Press, 2013
Progress in molecular biology and translational science ; v. 114