BETA CELLS: FUNCTIONS, PATHOLOGY AND RESEARCH -- BETA CELLS: FUNCTIONS, PATHOLOGY AND RESEARCH -- Library of Congress Cataloging-in-Publication Data -- Contents -- Preface -- Chapter I Stress and Pancreatic β Cell Function: Role of Glucocortoids, Exercise and Glucolipotoxicity -- Abstract -- Introduction -- β Cell Adaptation -- β Cell Mass in Obesity -- Life Cycle of the β Cell -- Glucocorticoids and β Cell Function -- Direct Effects of Glucocorticoids on β Cells -- Indirect Effects of Glucocorticoids on β Cell Function -- Role of GRs on β Cell Survival and Replication -- Intermittent Stress and β Cell Function -- Exercise Intervention on β Cell Function -- Exercise Causes Pancreatic Regeneration in Partial Pancreatectomy Models -- Disposition Index on β Cell Function -- Age and Exercise on β Cell Function -- Glucolipotoxicity on β Cell Function -- Glucotoxicity -- Lipotoxicity -- Short Term Effects of FFAs -- Long Term Effects of FFAs -- FFAs and ER Stress -- Conclusion -- References -- Chapter II The Synergistic Effect of β Cell Replacement and Immunotherapy on the Treatment of Type 1 Diabetes -- Abstract -- Introduction -- β-Cell Replacement -- Patient-Specific ß-Cells -- 1. Autologous adult stem cell-derived ß-cells -- 2. Induced pluripotent stem cells -- 3. Transdifferentiation-induced β-like cells -- Embryonic Stem Cell-Derived ß-Cells -- Islet Transplantation -- Pancreas Transplantation -- Immunotherapy -- Immunopathology of T1D -- Treg-Based Immunotherapy -- 1. Evidence of Treg function in the control of T1D -- 2. Mechanisms of Treg function in T1D -- 3. Therapeutic potential of Tregs on T1D -- Antigen/ Antibody-Based Immunotherapy -- The Potential Synergistic Role of β-Cell Replacement and Immunotherapy -- 1. Bi-Directional Actions of Cell-Based Therapy -- 2. Multiple Functions of Immunotherapy.

3. Temporal and Spatial Actions of Immunotherapy -- Summary and Conclusion -- Acknowledgments -- References -- Chapter III Antagonizing the Endocannabinoid Pathway Prevents the Development of Diabetes and β Cell Dysfunction in Zucker Diabetic Fatty Rats -- Abstract -- Methods -- Results -- Introduction -- Materials and Methods -- I. Drugs and Reagents -- II. Animals -- III. Treatment and Follow-up -- IV. Islet Isolation -- V. Glucose-Stimulated Insulin Secretion (GSIS) Assessment by Static Incubation of Isolated ZDF Rat Islets -- VI. Glucose-Stimulated Insulin Secretion (GSIS) Assessment by Perifusion of Isolated ZDF Rat Islets -- VII. Expression of Results and Statistical Analyses -- 1. Expression of the results -- 2. Statistical analyses -- Results -- I. Effect of Rimonabant Administration (10 Mg/Kg/D) on Body Weight of ZDF Rats -- II. Rimonabant Administration (10 Mg/Kg/D) Prevents the Elevation of Blood Glucose Levels of ZDF Rats -- III. Rimonabant Administration (10 Mg/Kg/D) Reduces the Decline of Insulinemia of ZDF Rats -- IV. Rimonabant Administration (10 Mg/Kg/D) Reduces ( Cell Dysfunction in ZDF Rats -- 1. Insulin secretion during static incubation of islets isolated from ZDF rats treated for 2 weeks -- 2. Insulin secretion during static incubation of islets isolated from ZDF rats treated for 6 weeks -- 3. Insulin secretion during perifusion of islets isolated from ZDF rats treated for 2 weeks -- 4. Insulin secretion during perifusion of islets isolated from ZDF rats treated for 6 weeks -- Discussion -- Conclusion -- Acknowledgments -- References -- Chapter IV Diabetes Mellitus: An Opportunity for Therapy with Regenerative Medicine? -- Abstract -- Introduction -- Pancreatic Islet as a Miniorgan -- Islet Transplantation -- Differentiation of Islet Cells during Embryonic Development -- Revisit to "Stem Cells" -- Totipotent Stem Cells.

Use of Adult Precursor Cells for Therapeutic Modalities -- Summary -- Conclusion -- Acknowledgments -- References -- Chapter V Behind Beta Cell Glucotoxicity: A Pivotal Role of Glycoxidative Damage? -- Abstract -- Introduction -- Glucotoxicity -- Formation and Accumulation of AGEs -- AGEs and Diabetes -- AGEs and Beta Cells -- AGEs, (-cells and oxidative stress -- AGEs and (-cell survival -- AGEs and Insulin Secretion -- AGEs and β-cell insulin production -- Conclusion -- References -- Chapter VI Induction of Pancreatic Cancer Cell Death by Elevated Concentrations of Extracellular Zinc -- Abstract -- Introduction -- Differential Sensitivity of Untransformed and Cancerous Pancreatic Cells to Exogenous Zinc -- Altered Zinc Homeostasis in Pancreatic Cancer Cells -- Mechanisms of Zinc-Induced Cytotoxicity in Pancreatic Cancer Cells -- Conclusion -- References -- Chapter VII Rab GTPases Control Membrane Recycling in the Pancreatic Beta Cell -- Abstract -- Introduction -- 1. Stages of Insulin Secretion -- 2. The Small GTPase Rab -- 3. Rab3 and Rab27a Effectors -- Perspectives -- Footnotes -- References -- Chapter VIII In Vivo Reprogramming of Pancreatic -cells into β-like Cells -- Acknowledgments -- References -- Chapter IX Studies of Toxin Resistant Beta-Cells: Lessons for the Chemotherapy? -- Abstract -- Introduction -- The Mechanisms of Beta-Cell Death -- Model 1. The Okamoto Model -- Model 2. The Activation of Apoptosis Cascades -- Studies of multitoxin resistant cells -- Group 1- Alloxan/Ninhydrin/ Hydrogen Peroxide -- The Story of Alloxan/Ninhydrin/Hydrogen Peroxide Resistant Cells: RINmA/ BRINnt/RINmHP Cells -- Group 2- Streptozotocin -- The Story of Streptozotocin Resistant RINmS and BRINst Cells -- Group 3- Cytokines -- The Story of Cytokine Resistant Cell Line: INSres Cells -- "Stemness" of Those Toxin Resistant Cells -- Conclusion.

References -- Chapter X Renin-Angiotensin System and Diabetes -- Abstract -- Abbreviations -- Introduction to Diabetes -- Introduction to the RAS -- RAS in Beta-Cells -- RAS Blockers as Therapeutic Agents to Control Diabetes -- ACE2: A Potential Therapeutic Target to Control Ang-II-Mediated Type 2 Diabetes -- Ang (1-7) and Mas Signaling -- Perspective -- References -- Index.