Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fridlyand, L. E.
Right arrow Articles by Philipson, L. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fridlyand, L. E.
Right arrow Articles by Philipson, L. H.
Social Bookmarking
Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes 53:1942-1948, 2004
© 2004 by the American Diabetes Association, Inc.

Perspectives in Diabetes

Does the Glucose-Dependent Insulin Secretion Mechanism Itself Cause Oxidative Stress in Pancreatic ß-Cells?

Leonid E. Fridlyand, and Louis H. Philipson

From the Department of Medicine, University of Chicago, Chicago, Illinois

Glucose-dependent insulin secretion (GDIS), reactive oxygen species (ROS) production, and oxidative stress in pancreatic ß-cells may be tightly linked processes. Here we suggest that the same pathways used in the activation of GDIS (increased glycolytic flux, ATP-to-ADP ratio, and intracellular Ca2+ concentration) can dramatically enhance ROS production and manifestations of oxidative stress and, possibly, apoptosis. The increase in ROS production and oxidative stress produced by GDIS activation itself suggests a dual role for metabolic insulin secretagogues, as an initial sharp increase in insulin secretion rate can be accompanied by progressive ß-cell injury. We propose that therapeutic strategies targeting enhancement of GDIS should be carefully considered in light of possible loss of ß-cell function and mass.

Address correspondence and reprint requests to Louis H. Philipson, Department of Medicine, MC 1027, University of Chicago, 5841 S. Maryland Ave., Chicago, IL 60637. E-mail: l-philipson{at}uchicago.edu


Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 DiabetesHome page
J. Pi, Y. Bai, Q. Zhang, V. Wong, L. M. Floering, K. Daniel, J. M. Reece, J. T. Deeney, M. E. Andersen, B. E. Corkey, et al.
Reactive Oxygen Species as a Signal in Glucose-Stimulated Insulin Secretion
Diabetes, July 1, 2007; 56(7): 1783 - 1791.
[Abstract] [Full Text] [PDF]

Home page
 Diabetes CareHome page
T. A. Buchanan, A. Xiang, S. L. Kjos, and R. Watanabe
What Is Gestational Diabetes?
Diabetes Care, July 1, 2007; 30(Supplement_2): S105 - S111.
[Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
K. Kitiphongspattana, T. A. Khan, K. Ishii-Schrade, M. W. Roe, L. H. Philipson, and H. R. Gaskins
Protective role for nitric oxide during the endoplasmic reticulum stress response in pancreatic beta-cells
Am J Physiol Endocrinol Metab, June 1, 2007; 292(6): E1543 - E1554.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
Z. Ma, N. Portwood, D. Brodin, V. Grill, and A. Bjorklund
Effects of Diazoxide on Gene Expression in Rat Pancreatic Islets Are Largely Linked to Elevated Glucose and Potentially Serve to Enhance {beta}-Cell Sensitivity
Diabetes, April 1, 2007; 56(4): 1095 - 1106.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
C. Leloup, C. Magnan, A. Benani, E. Bonnet, T. Alquier, G. Offer, A. Carriere, A. Periquet, Y. Fernandez, A. Ktorza, et al.
Mitochondrial reactive oxygen species are required for hypothalamic glucose sensing.
Diabetes, July 1, 2006; 55(7): 2084 - 2090.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
M. Z. Khaldi, H. Elouil, Y. Guiot, J. C. Henquin, and J. C. Jonas
Antioxidants N-acetyl-L-cysteine and manganese(III)tetrakis (4-benzoic acid)porphyrin do not prevent beta-cell dysfunction in rat islets cultured in high glucose for 1 wk
Am J Physiol Endocrinol Metab, July 1, 2006; 291(1): E137 - E146.
[Abstract] [Full Text] [PDF]

Home page
 Ann. N. Y. Acad. Sci.Home page
L. E. FRIDLYAND and L. H. PHILIPSON
Oxidative Reactive Species in Cell Injury: Mechanisms in Diabetes Mellitus and Therapeutic Approaches
Ann. N.Y. Acad. Sci., December 1, 2005; 1066(1): 136 - 151.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
M. Cnop, N. Welsh, J.-C. Jonas, A. Jorns, S. Lenzen, and D. L. Eizirik
Mechanisms of Pancreatic {beta}-Cell Death in Type 1 and Type 2 Diabetes: Many Differences, Few Similarities
Diabetes, December 1, 2005; 54(suppl_2): S97 - S107.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
L. E. Fridlyand, L. Ma, and L. H. Philipson
Adenine nucleotide regulation in pancreatic {beta}-cells: modeling of ATP/ADP-Ca2+ interactions
Am J Physiol Endocrinol Metab, November 1, 2005; 289(5): E839 - E848.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
G. A. Martens, Y. Cai, S. Hinke, G. Stange, M. Van de Casteele, and D. Pipeleers
Glucose Suppresses Superoxide Generation in Metabolically Responsive Pancreatic {beta} Cells
J. Biol. Chem., May 27, 2005; 280(21): 20389 - 20396.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 2004 by the American Diabetes Association.