Document Detail


DPP-4 inhibition increases GIP and decreases GLP-1 incretin effects during intravenous glucose tolerance test in Wistar rats.
MedLine Citation:
PMID:  21281062     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
Abstract GIP metabolite [GIP (3-42)] and GLP-1 metabolite [GLP-1 (9-36) amide] have been reported to differ with regard to biological actions. Systemic DPP-4 inhibition can therefore reveal different actions of GIP and GLP-1. In catheter wearing Wistar rats, insulinotropic effects of equipotent doses of GIP (2.0 nmol/kg) and GLP-1 (7-36) amide (4.0 nmol/kg) and vehicle were tested in the absence/presence of DPP-4 inhibition. Blood glucose and insulin were frequently sampled. DPP-4 inhibitor was given at -20 min, the incretin at -5 min and the intravenous glucose tolerance test (0.4 g glucose/kg) commenced at 0 min. G-AUC and I-AUC, insulinogenic index and glucose efflux, were calculated from glucose and insulin curves. Systemic DPP-4 inhibition potentiated the acute GIP incretin effects: I-AUC (115±34 vs. 153±39 ng·min/ml), increased the insulinogenic index (0.74±0.24 vs. 0.99±0.26 ng/mmol), and improved glucose efflux (19.8±3.1 vs. 20.5±5.0 min(-1)). The GLP-1 incretin effects were diminished: I-AUC (124±18 vs. 106±38 ng·min/ml), the insulinogenic index was decreased (0.70±0.18 vs. 0.50±0.19 ng/mmol), and glucose efflux declined (14.9±3.1 vs. 11.1±3.7 min(-1)). GLP-1 and GIP differ remarkably in their glucoregulatory actions in healthy rats when DPP-4 is inhibited. These previously unrecognized actions of DPP-4 inhibitors could have implications for future use in humans.
Authors:
Ernst-Joachim Freyse; Sabine Berg; Klaus-Dieter Kohnert; Peter Heinke; Eckhard Salzsieder
Publication Detail:
Type:  Journal Article     Date:  2011-01-31
Journal Detail:
Title:  Biological chemistry     Volume:  392     ISSN:  1437-4315     ISO Abbreviation:  Biol. Chem.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2011-02-04     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9700112     Medline TA:  Biol Chem     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  209-15     Citation Subset:  IM    
Affiliation:
Institute of Diabetes 'Gerhardt Katsch' Karlsburg, D-17495 Karlsburg, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

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


Previous Document:  Phaeohyphomycosis caused by a plant pathogen, Corynespora cassiicola.
Next Document:  A novel thermodynamic treatment for meibomian gland dysfunction.