Beta cells : functions, pathology, and research / Sarah E. Gallagher, editor.

Format:

Book

Contributor:

Gallagher, S.

Series:

Cell Biology Research Progress

Cell biology research progress

Language:

English

Subjects (All):

Pancreatic beta cells.

Diabetes.

Physical Description:

1 online resource (190 p.)

Edition:

1st ed.

Place of Publication:

New York : Nova Science Publishers, c2011.

Language Note:

English

Summary:

Beta cells or ss-cells, are a type of cell in the pancreas in areas called the islets of Langerhans. This book presents research from across the globe in the study of Beta-cells, including the induction of pancreatic cancer cell death by elevated concentrations of extracellular zinc.

Contents:

Intro

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

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

Chapter III Antagonizing the Endocannabinoid Pathway Prevents the Development of Diabetes and β Cell Dysfunction in Zucker Diabetic Fatty Rats

Methods

Results

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

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

Chapter IV Diabetes Mellitus: An Opportunity for Therapy with Regenerative Medicine?

Pancreatic Islet as a Miniorgan

Differentiation of Islet Cells during Embryonic Development

Revisit to "Stem Cells"

Totipotent Stem Cells.

Use of Adult Precursor Cells for Therapeutic Modalities

Summary

Chapter V Behind Beta Cell Glucotoxicity: A Pivotal Role of Glycoxidative Damage?

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

Chapter VI Induction of Pancreatic Cancer Cell Death by Elevated Concentrations of Extracellular Zinc

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

Chapter VII Rab GTPases Control Membrane Recycling in the Pancreatic Beta Cell

1. Stages of Insulin Secretion

2. The Small GTPase Rab

3. Rab3 and Rab27a Effectors

Perspectives

Footnotes

Chapter VIII In Vivo Reprogramming of Pancreatic -cells into β-like Cells

Chapter IX Studies of Toxin Resistant Beta-Cells: Lessons for the Chemotherapy?

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

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

Index.

Notes:

Description based upon print version of record.

Includes bibliographical references and index.

Description based on print version record.

ISBN:

1-61761-372-X

OCLC:

847655087