Document Detail


Functional pancreatic beta-cell mass: involvement in type 2 diabetes and therapeutic intervention.
MedLine Citation:
PMID:  19251449     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the adult, the pancreatic beta-cell mass adapts insulin secretion to meet long-term changes in insulin demand and, in particular, in the presence of insulin resistance that is either physiological, such as pregnancy, or pathophysiological, such as obesity. The failure of beta cells to compensate for insulin resistance is a major component of impaired glucose homeostasis and overt diabetes. This defect is clearly the consequence of a decline of insulin response to glucose due to functional beta-cell deficiency. It is also the consequence of an inability of the endocrine pancreas to adapt the beta-cell mass to insulin demand (pancreas plasticity), which eventually leads to a decrease in functional beta-cell mass. This idea has resulted in considerable attention being paid to the development of new therapeutic strategies aiming to preserve and/or regenerate functional beta-cell mass. The latter is governed by a constant balance between beta-cell growth (replication from pre-existing beta cells and neogenesis from precursor cells) and beta-cell death (mainly apoptosis). Disruption of this balance may lead to rapid and marked changes in beta-cell mass. Glucagon-like peptide-1 (GLP-1), an incretin, enhances beta-cell survival (by activating beta-cell proliferation and differentiation, and inhibiting beta-cell apoptosis), thus contributing to the long-term regulation of insulin secretion by maintaining a functional beta-cell mass. The development of drugs regulating this parameter will be the major challenge of the next few years in the management of type 2 diabetes.
Authors:
M Karaca; C Magnan; C Kargar
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Publication Detail:
Type:  Journal Article; Review     Date:  2009-02-28
Journal Detail:
Title:  Diabetes & metabolism     Volume:  35     ISSN:  1262-3636     ISO Abbreviation:  Diabetes Metab.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-14     Completed Date:  2009-08-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9607599     Medline TA:  Diabetes Metab     Country:  France    
Other Details:
Languages:  eng     Pagination:  77-84     Citation Subset:  IM    
Affiliation:
Université Paris-Diderot, 75205 Paris cedex 13, France. meliskaraca@gmail.com
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Antigens, CD26 / antagonists & inhibitors
Diabetes Mellitus, Type 2 / drug therapy*,  physiopathology*
Glucagon-Like Peptide 1 / analogs & derivatives,  physiology*,  therapeutic use
Humans
Incretins / physiology*,  therapeutic use
Insulin Resistance
Insulin-Secreting Cells / cytology,  physiology*
Chemical
Reg. No./Substance:
0/Incretins; 89750-14-1/Glucagon-Like Peptide 1; EC 3.4.14.5/Antigens, CD26; EC 3.4.14.5/DPP4 protein, human

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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