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Glucose Homeostatis and the Pathogenesis of Diabetes Mellitus /

Diabetes mellitus is a disease with tremendous health and economic burden. A better understanding of how normal glucose homeostasis is maintained and the pathogenesis is important to identify new ways for diabetes treatment. This book addresses multiple aspects of this area of research. Key features...

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Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Tao, Ya-Xiong
Formato: Electrónico eBook
Idioma:Inglés
Publicado: London : Academic Press, �2014.
Edición:First edition.
Colección:Progress in molecular biology and translational science ; v. 121.
Temas:
Acceso en línea:Texto completo
Texto completo

MARC

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245 0 0 |a Glucose Homeostatis and the Pathogenesis of Diabetes Mellitus /  |c edited by Ya-Xiong Tao. 
250 |a First edition. 
260 |a London :  |b Academic Press,  |c �2014. 
300 |a 1 online resource (xvi, 486 pages) :  |b illustrations 
336 |a text  |b txt  |2 rdacontent 
337 |a computer  |b c  |2 rdamedia 
338 |a online resource  |b cr  |2 rdacarrier 
490 1 |a Progress in molecular biology and translational science,  |x 1877-1173 ;  |v v. 121 
500 |a Title from PDF title page (Science Direct, viewed January 7, 2014). 
504 |a Includes bibliographical references and index. 
505 0 |a Front Cover; Glucose Homeostatis and the Pathogenesis of Diabetes Mellitus; Copyright; Contents; Contributors; Preface; Chapter One: G Protein-Coupled Receptors as Regulators of Glucose Homeostasis and Therapeutic Targets for Diabetes Mellitus; 1. Introduction; 2. Regulation of Glucose Homeostasis by GPCRs in the Central Nervous System; 3. Regulation of Glucose Homeostasis by GPCRs for Peptides from Endocrine Pancreas; 4. Regulation of Insulin Secretion by GPCRs; 5. Regulation of Incretin Secretion by GPCRs; 6. Regulation of Glucose Homeostasis by Orphan GPCRs; 7. Summary; Acknowledgments 
505 8 |a 12. Safety Considerations for GLP-1-Based Therapeutics13. Conclusion; Acknowledgments; References; Chapter Three: Physiology and Therapeutics of the Free Fatty Acid Receptor GPR40; 1. Introduction; 2. Molecular Cloning and Tissue Distribution of GPR40; 2.1. Molecular cloning; 2.2. Tissue distribution; 3. Physiology of GPR40; 3.1. Insulin secretion and glucolipotoxicity; 3.2. Incretin secretion; 3.3. Glucagon secretion; 3.4. Inflammation; 3.5. Bone density; 3.6. Neurogenesis and pain control; 3.7. Cell proliferation; 3.8. Taste preference; 4. Pharmacology of GPR40 
505 8 |a 4. Pharmacology of GPR1194.1. Ligand development and receptor activation; 4.2. Signaling pathways and regulation; 5. Conclusions; Acknowledgments; References; Chapter Five: Enhanced Skeletal Muscle for Effective Glucose Homeostasis; 1. Introduction; 2. Skeletal Muscle and Glucose Homeostasis; 3. Skeletal Muscle Formation; 4. Myogenic Regulatory Factors; 5. Postnatal Development of Skeletal Muscle; 6. Myostatin and Skeletal Muscle Mass; 7. Enhanced Muscle Growth for Preventing Diabetes; 8. Concluding Remarks; Acknowledgments; References 
520 |a Diabetes mellitus is a disease with tremendous health and economic burden. A better understanding of how normal glucose homeostasis is maintained and the pathogenesis is important to identify new ways for diabetes treatment. This book addresses multiple aspects of this area of research. Key features: * Written by experts in the field * Informs on important topics related to the regulation of glucose homeostasis and the pathogenesis of diabetes mellitus, a field of intense research interest. 
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650 0 |a Glucose. 
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650 2 |a Glucose  |0 (DNLM)D005947 
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650 7 |a Homeostasis  |2 fast  |0 (OCoLC)fst00959606 
700 1 |a Tao, Ya-Xiong. 
776 0 8 |i Print version:  |t Glucose homeostatis and the pathogenesis of diabetes mellitus.  |b First edition.  |d Oxford, [England] : Academic Press, �2014  |h xvi, 486 pages  |k Progress in molecular biology and translational science ; Volume 121  |x 1877-1173  |z 9780128001011 
830 0 |a Progress in molecular biology and translational science ;  |v v. 121. 
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856 4 0 |u https://sciencedirect.uam.elogim.com/science/bookseries/18771173/121  |z Texto completo