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Current and future developments in physiology. Volume 1 : control of pancreatic beta cell function and plasticity in health and diabetes / edited by David J. Hill.
EBSCOhost Academic eBook Collection (North America) Available online
EBSCOhost Academic eBook Collection (North America)- Format:
- Book
- Author/Creator:
- Hill, David J, Author.
- Series:
- Current and Future Developments in Physiology, 2468-7537 ; Volume 1
- Language:
- English
- Subjects (All):
- Physiology.
- Physiology--Congresses.
- Physical Description:
- 1 online resource (253 pages) : illustrations (some color).
- Edition:
- 1st ed.
- Place of Publication:
- Sharjah, United Arab Emirates : Bentham Books, 2016.
- Summary:
- Plasticity in insulin-producing cells (β-cells) of the pancreas is a major contributor to metabolic control. Targeted regeneration of pancreatic β-cells for the reversal of diabetes (by optimizing β-cells mass and proliferation to meet metabolic requirements and counter autoimmune response) is still a theoretical intervention. This monograph reviews the biology, ontogeny, capabilities, and present practical limitations of β-cell plasticity. Relevant biochemical pathways are described with the inclusion of information about how they change with aging, during pregnancy, and with diet. Readers will learn the following key aspects about β-cell plasticity: -current knowledge of pancreatic β-cells development, and how β-cell mass and proliferation change throughout the human lifespan -the mechanisms responsible for β-cell plasticity, based on animal models and clinical studies revealing environmental, epigenetic, endocrine and paracrine regulators -the therapeutic potential of resident stem cells within the pancreas / bone marrow and β-cell progenitors This monograph is essential reading for researchers interested in updated knowledge about the molecular and cellular biology of β-cells in the quest to find a reliable therapy for diabetes.
- Contents:
- Intro
- CONTENTS
- FOREWORD
- REFERENCES
- PREFACE
- List of Contributors
- Section 1: Origins and Developmental Biology of β-Cells
- Understanding the Developmental Biology of β-Cells as a Strategy for Diabetes Reversal
- GENETIC NETWORK CONTROLLING PANCREATIC DEVELOPMENT
- The Sequential Implication of Transcription Factors
- THE PANCREATIC MESENCHYME AND GROWTH FACTORS
- ROLE OF NUTRIENTS IN THE DEVELOPMENT OF Β-CELLS
- Impact of Protein Levels
- The Effects of Glucose
- IMPORTANCE OF THE PARTIAL PRESSURE OF OXYGEN IN THE INTRAUTERINE MILIEU
- OXIDATIVE STRESS AND Β-CELL DEVELOPMENT
- FROM DEVELOPMENTAL BIOLOGY STUDIES TO INNOVATIVE THERAPEUTIC STRATEGIES FOR THE TREATMENT OF DIABETES
- The Context of Diabetes
- Application of Our Knowledge From β-Cell Development to Treating Diabetes
- Type 1 Diabetes and Islet Transplantation
- THE GENETICS OF PANCREAS EMBRYOGENESIS AND THE OCCURRENCE OF DIABETES
- CONFLICT OF INTEREST
- ACKNOWLEDGEMENTS
- Aging and β-Cell Proliferation, Molecular and Signaling Changes and What This Means for Targeted Regeneration
- AGING AND DIABETES
- Β-CELL PROLIFERATION AND AGING
- AGING AND ADAPTIVE Β-CELL PROLIFERATION
- MOLECULAR AND SIGNALING CHANGES IN AGING
- SIGNIFICANCE FOR TARGETED Β-CELL REGENERATION
- Human β-Cell Mass and Distribution in Health, Aging and Diabetes
- INTRODUCTION
- HUMAN PANCREAS
- Anatomy
- Regional Differences in β-Cell/Islet Mass
- The Head of the Pancreas
- Islet Architecture and Cellular Composition
- Β-CELL MASS IN AGING AND DIABETES
- Absolute Mass of β-Cells and Islets in Humans
- β-Cell Mass in Aging and Obesity
- Loss of β-Cell Mass in Diabetes
- Physical vs. Functional Loss of β-Cell Mass
- WHOLE PANCREAS ANALYSIS
- CONCLUDING REMARKS.
- CONFLICT OF INTEREST
- Section 2: Factors Controlling β-Cell Mass and Function
- Gestational Programming of β-Cell Mass and Pancreatic Function in the Next Generation
- ANIMAL MODELS OF FETAL PROGRAMMING OF THE ENDOCRINE PANCREAS THROUGH NUTRITIONAL DEFICIT
- ANIMAL MODELS OF FETAL PROGRAMMING OF THE ENDOCRINE PANCREAS THROUGH HYPERGLYCEMIA
- MECHANISMS OF FETAL PROGRAMMING OF THE PANCREATIC FUNCTION
- Early Dietary Insult and the mTOR Axis
- Epigenetic Mechanisms Governing Pancreatic Gene Expression and Their Involvement in Fetal Programming of Metabolic Disease
- Epigenetic Changes to Pancreatic Gene Expression Caused by Environmental Toxins
- Prematurity of Cellular Aging
- REVERSAL STRATEGIES FOR FETAL PROGRAMMING OF THE PANCREAS
- CONCLUSION
- Malprogramming of β-Cell Function by a Dietary Modification in the Immediate Postnatal Period
- Metabolic Programming After Birth
- EXPERIMENTAL APPROACHES: 'PUP-IN-A-CUP' RAT MODEL
- Alterations in Islets Mass
- Molecular Adaptations
- MOLECULAR MECHANISM BY WHICH GLUCOSE CAN CONTROL Β-CELL MASS
- Alterations in Nutrient-Mediated Insulin Secretion
- Alterations in Non-Nutrient-Mediated Insulin Secretion
- Long-Term Consequences Due to Programming
- IS IT POSSIBLE TO REVERSE METABOLIC PROGRAMMING IN ADULTHOOD?
- RELEVANCE TO OBESITY AND TYPE 2 DIABETES
- New Concepts in the Intra-Islet Control of β-Cell Function and Mass
- Defining the Importance of β-Cell Function and Mass
- Known Factors Affecting β-Cell Function and Mass and Their Mode of Action
- PARACRINE AND AUTOCRINE FACTORS REGULATING Β-CELL FUNCTION.
- Anatomic Differences Affect Paracrine and Autocrine Signaling Properties Between Species
- Emerging Autocrine Factors
- Insulin
- Proinsulin C-Peptide
- Islet Amyloid Polypeptide
- GABA
- Serotonin
- Nicotonic Acid Adenine Dinucleotide Phosphate (NAADP)
- Cholecystokinin (CCK)
- Acetate
- Emerging Paracrine Factors
- Acetylcholine
- VGF-Derived Peptides
- Approaches to Identify New Autocrine/Paracrine Signaling Factors
- β-Cell Adaptability During Pregnancy
- Morphological Changes
- Hormonal Changes During Pregnancy
- Somatolactogenic Hormones - Systemic Effects
- Somatolactogenic Hormones - Lessons from In Vitro Studies
- Somatolactogenic Hormones - Lessons from Transgenic Mice
- Somatolactogenic Hormones - Mechanism of Action
- Somatolactogenic Hormones - A Downstream Role of STAT5
- Role of Glucocorticoid Hormones
- Role of Progesterone
- Role of Estrogens
- Role of Epidermal Growth Factor (EGF)
- Role of Nerve Growth Factor (NGF)
- Role of Hepatocyte Growth Factor (HGF)
- Role of Survivin
- Role of IGF-Binding Protein 5 (Igfbp5)
- Role of Glucagon-like Peptide 1 (Glp-1)
- Role of Glucose and Fatty Acids
- Role on Neurogenin 3 (Ngn-3)
- Role of Forkhead Box Protein M1 (FoxM1)
- Role of Hepatic Nuclear Factor 4α (Hnf4α)
- Role of B-cell Lymphoma 6 Protein Homolog (Bcl6) and Menin (Men1)
- Role of Betatrophin
- Role of Osteoprotegerin (OPG)
- Role of Serotonin
- Role of Cyclophilin B
- Role of Stathmins
- Role of Delta-like 1 (dlk-1)
- Role of Trefoil Factors (TFF)
- Other Differentially Expressed Islet Genes
- Circulating Factors in Pregnancy that may Influence β-Cell Function
- Diabetes in Pregnancy
- β-Cell Adaptation Postpartum
- REFERENCES.
- Section 3: Generation of β-Cells and Future Applications
- β-Cells from Embryonic and Adult Stem Cells and Progenitors
- GENERATION OF Β-CELLS FROM STEM CELL SOURCE
- REGENERATION OF THE ENDOCRINE PANCREAS
- Generation of Insulin-Expressing Cells In Vitro
- Resident Stem/Progenitor Cells Within the Endocrine Pancreas
- Promiscuity in Cell Lineage Within the Endocrine Pancreas
- Induction of β-Cell Regeneration by Human Postnatal Stem Cells
- Dealing with the Complications and Consequences of Diabetes Mellitus: An Emerging Global Crisis?
- The Advent of Cellular Therapies for Diabetes: The Edmonton Protocol
- Can Islet Regeneration Occur in the Face of Autoimmunity: The Medalist Study?
- Bone Marrow Stem Cells Initiate Islet Regeneration: Identifying the Mechanisms?
- HEMATOPOIETIC STEM AND PROGENITOR CELLS
- Why Use HPC for Islet Regeneration?
- Isolation of Human Hematopoietic Progenitor Cells Using High ALDH-Activity
- Preclinical Xenotransplantation Models to Investigate Islet Regeneration
- Human HPC with High ALDH-activity Promote Regenerating Islet Cell Proliferation and Vascularization
- Islet Regenerative Functions by Expanded HPC Subsets with High ALDH-Activity
- Can HPC Transplantation Abrogate Autoimmunity and Permit Endogenous Islet Regeneration?
- MULTIPOTENT MESENCHYMAL STROMAL CELLS (MSC)
- Can MSC Create a Regenerative Niche for New Islet Formation?
- MSC Immunomodulation and Recruitment of M2 Macrophages to Promote Islet Regeneration
- Can MSC Reverse Autoimmunity in T1D and Support Endogenous β-Cell Regeneration?
- ENDOTHELIAL PROGENITOR CELLS (EPC)
- Can We Utilize EPC to Support Endogenous Islet Regeneration and Revascularization?
- EPC-induced Vascularization Support the Survival and Function of Islet Allografts?.
- CONCLUSION AND FUTURE DIRECTIONS
- SUBJECT INDEX.
- Notes:
- Includes bibliographical references at the end of each chapters and index.
- Description based on online resource; title from PDF title page (Ebrary, viewed December 23, 2016).
- ISBN:
- 9781681083650
- 1681083655
- OCLC:
- 969638692
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