| The contribution of enteroinsular hormones to the pathogenesis of type 2 diabetes mellitus. | |
| | |
MedLine Citation:
|
PMID: 20425582 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
The gastrointestinal hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), termed incretins, are essential regulators of normal glucose homeostasis. Research indicates that the incretin effect is impaired in type 2 diabetes, and this seems to be a consequence rather than a cause of type 2 diabetes. This review describes the defects in the incretin system seen in diabetic patients and discusses the potential roles of GIP and GLP-1 in the pathogenesis of type 2 diabetes. In addition, new information on clinical applications that exploit the enteroinsular axis to control blood glucose is discussed. |
| | |
Authors:
|
Dima L Diab; David A D'Alessio |
Publication Detail:
|
Type: Journal Article; Review |
Journal Detail:
|
Title: Current diabetes reports Volume: 10 ISSN: 1539-0829 ISO Abbreviation: Curr. Diab. Rep. Publication Date: 2010 Jun |
Date Detail:
|
Created Date: 2010-04-28 Completed Date: 2010-09-14 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 101093791 Medline TA: Curr Diab Rep Country: United States |
Other Details:
|
Languages: eng Pagination: 192-8 Citation Subset: IM |
Affiliation:
|
Division of Endocrinology/Metabolism, Cincinnati VA Medical Center, University of Cincinnati, ML 0547, Vontz Center, Cincinnati, OH 45220-0547, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Diabetes Mellitus, Type 2 / drug therapy, etiology* Gastrointestinal Hormones / metabolism* Humans Hypoglycemic Agents / therapeutic use Incretins / metabolism Insulin / metabolism* |
| Chemical | |
Reg. No./Substance:
|
0/Gastrointestinal Hormones; 0/Hypoglycemic Agents; 0/Incretins; 11061-68-0/Insulin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Defects in insulin secretion and action in the pathogenesis of type 2 diabetes mellitus.
Next Document: Metabolic syndrome in blacks: are the criteria right?