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http://purl.uniprot.org/citations/19327106http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19327106http://www.w3.org/2000/01/rdf-schema#comment"

Background

Treatment of diabetes type 2 using chronic pharmacological inhibition of dipeptidyl peptidase 4 (DP4) still requires an in-depth analysis of models for chronic DP4 deficiency, because adverse reactions induced by some DP4 inhibitors have been described.

Methods

In the present study, a novel congenic rat model of DP4 deficiency on a "DP4-high" DA rat genetic background was generated (DA.F344-Dpp4(m)/ SvH rats) and comprehensively phenotyped.

Results

Similar to chronic pharmacological inhibition of DP4, DP4 deficient rats exhibited a phenotype involving reduced diet-induced body weight gain and improved glucose tolerance associated with increased levels of glucagon-like peptide-1 (GLP-1) and bound leptin as well as decreased aminotransferases and triglycerides. Additionally, DA.F344-Dpp4(m)/SvH rats showed anxiolytic-like and reduced stress-like responses, a phenomenon presently not targeted by DP4 inhibitors. However, several immune alterations, such as differential leukocyte subset composition at baseline, blunted natural killer cell and T-cell functions, and altered cytokine levels were observed.

Conclusions

While this animal model confirms a critical role of DP4 in GLP-1-dependent glucose regulation, genetically induced chronic DP4 deficiency apparently also affects stress-regulatory and immuneregulatory systems, indicating that the use of chronic DP4 inhibitors might have the potential to interfere with central nervous system and immune functions in vivo."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.org/dc/terms/identifier"doi:10.1515/cclm.2009.064"xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Wagner L."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"von Horsten S."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Hoffmann T."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Demuth H.U."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Stephan M."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Jacobs R."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Forssmann U."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Brabant G."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Bode F."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Klemann C."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Wedekind D."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Straub R.H."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Jorns A."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Nave H."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Pabst R."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Skripuletz T."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Schade J."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Frerker N."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Johannes S."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/author"Raber K."xsd:string
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19327106http://purl.uniprot.org/core/name"Clin Chem Lab Med"xsd:string
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