help button home button Endocrine Society Endocrine Reviews
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrine Reviews, doi:10.1210/er.2007-0031
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow RPHR Note
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Salehi, M.
Right arrow Articles by D'Alessio, D. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Salehi, M.
Right arrow Articles by D'Alessio, D. A.
Endocrine Reviews 29 (3): 367-379
Copyright © 2008 by The Endocrine Society

Targeting β-Cell Mass in Type 2 Diabetes: Promise and Limitations of New Drugs Based on Incretins

Marzieh Salehi, Benedikt A. Aulinger and David A. D'Alessio

Department of Medicine, Division of Endocrinology, University of Cincinnati, Cincinnati, Ohio 45267-0547

Correspondence: Address all correspondence and requests for reprints to: David D'Alessio, Department of Medicine, Division of Endocrinology, ML 0547, University of Cincinnati, Vontz Center for Molecular Studies, 3125 Eden Avenue, Cincinnati, Ohio 45267-0547. E-mail: dalessd{at}ucmail.uc.edu

Progressive insulin secretory defects, due to either functional abnormalities of the pancreatic β-cells or a reduction in β-cell mass, are the cornerstone of type 2 diabetes. Incretin-based drugs hold the potential to improve glucose tolerance by immediate favorable effect on β-cell physiology as well as by expanding or at least maintaining β-cell mass, which may delay the progression of the disease. Long-term studies in humans are needed to elaborate on these effects.




This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
S. B. Widenmaier, Z. Ao, S.-J. Kim, G. Warnock, and C. H. S. McIntosh
Suppression of p38 MAPK and JNK via Akt-mediated Inhibition of Apoptosis Signal-regulating Kinase 1 Constitutes a Core Component of the {beta}-Cell Pro-survival Effects of Glucose-dependent Insulinotropic Polypeptide
J. Biol. Chem., October 30, 2009; 284(44): 30372 - 30382.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
O. P. McGuinness, J. E. Ayala, M. R. Laughlin, and D. H. Wasserman
NIH experiment in centralized mouse phenotyping: the Vanderbilt experience and recommendations for evaluating glucose homeostasis in the mouse
Am J Physiol Endocrinol Metab, October 1, 2009; 297(4): E849 - E855.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. B. Widenmaier, A. V. Sampaio, T. M. Underhill, and C. H. S. McIntosh
Noncanonical Activation of Akt/Protein Kinase B in {beta}-Cells by the Incretin Hormone Glucose-dependent Insulinotropic Polypeptide
J. Biol. Chem., April 17, 2009; 284(16): 10764 - 10773.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
D. A. D'Alessio, A. M. Denney, L. M. Hermiller, R. L. Prigeon, J. M. Martin, W. G. Tharp, M. L. Saylan, Y. He, B. E. Dunning, J. E. Foley, et al.
Treatment with the Dipeptidyl Peptidase-4 Inhibitor Vildagliptin Improves Fasting Islet-Cell Function in Subjects with Type 2 Diabetes
J. Clin. Endocrinol. Metab., January 1, 2009; 94(1): 81 - 88.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2008 by The Endocrine Society