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http://purl.uniprot.org/citations/14988249http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/14988249http://www.w3.org/2000/01/rdf-schema#comment"Glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) are important factors in the pathogenesis of type 2 diabetes and have a promising therapeutic potential. Alterations of their secretion, in vivo degradation, and elimination in patients with chronic renal insufficiency (CRI) have not yet been characterized. Ten patients with CRI (aged 47 +/- 15 years, BMI 24.5 +/-2.2 kg/m(2), and serum creatinine 2.18 +/-0.86 mg/dl) and 10 matched healthy control subjects (aged 44 +/-12 years, BMI 24.9 +/- 3.4 kg/m(2), and serum creatinine 0.89 +/-0.10 mg/dl) were included. On separate occasions, an oral glucose tolerance test (75 g), an intravenous infusion of GLP-1 (0.5 pmol. kg(-1). min(-1) over 30 min), and an intravenous infusion of GIP (1.0 pmol. kg(-1). min(-1) over 30 min) were performed. Venous blood samples were drawn for the determination of glucose (glucose oxidase), insulin, C-peptide, GLP-1 (total and intact), and GIP (total and intact; specific immunoassays). Plasma levels of GIP (3-42) and GLP-1 (9-36 amide) were calculated. Statistics were performed using repeated-measures and one-way ANOVA. After the oral glucose load, plasma concentrations of intact GLP-1 and intact GIP reached similar levels in both groups (P = 0.31 and P = 0.87, respectively). The concentrations of GIP (3-42) and GLP-1 (9-36 amide) were significantly higher in the patients than in the control subjects (P = 0.0021 and P = 0.027, respectively). During and after the exogenous infusion, GLP-1 (9-36 amide) and GIP (3-42) reached higher plasma concentrations in the CRI patients than in the control subjects (P < 0.001 and P = 0.0033, respectively), whereas the plasma levels of intact GLP-1 and GIP were not different between the groups (P = 0.29 and P = 0.27, respectively). Plasma half-lives were 3.4 +/-0.6 and 2.3 +/- 0.4 min for intact GLP-1 (P = 0.13) and 5.3 +/- 0.8 and 3.3 +/-0.4 min for the GLP-1 metabolite (P = 0.029) for CRI patients vs. healthy control subjects, respectively. Plasma half-lives of intact GIP were 6.9 +/-1.4 and 5.0 +/- 1.2 min (P = 0.31) and 38.1 +/- 6.0 and 22.4 +/-3.0 min for the GIP metabolite (P = 0.032) for CRI patients vs. healthy control subjects, respectively. Insulin concentrations tended to be lower in the patients during all experiments, whereas C-peptide levels tended to be elevated. These data underline the importance of the kidneys for the final elimination of GIP and GLP-1. The initial dipeptidyl peptidase IV-mediated degradation of both hormones is almost unaffected by impairments in renal function. Delayed elimination of GLP-1 and GIP in renal insufficiency may influence the pharmacokinetics and pharmacodynamics of dipeptidyl peptidase IV-resistant incretin derivatives to be used for the treatment of patients with type 2 diabetes."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.org/dc/terms/identifier"doi:10.2337/diabetes.53.3.654"xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Gallwitz B."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Holst J.J."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Schmidt W.E."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Nauck M.A."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Deacon C.F."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Meier J.J."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Gaeckler D."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/author"Kranz D."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/name"Diabetes"xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/pages"654-662"xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/title"Secretion, degradation, and elimination of glucagon-like peptide 1 and gastric inhibitory polypeptide in patients with chronic renal insufficiency and healthy control subjects."xsd:string
http://purl.uniprot.org/citations/14988249http://purl.uniprot.org/core/volume"53"xsd:string
http://purl.uniprot.org/citations/14988249http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/14988249
http://purl.uniprot.org/citations/14988249http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/14988249
http://purl.uniprot.org/uniprot/#_P09681-mappedCitation-14988249http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14988249
http://purl.uniprot.org/uniprot/#_P01275-mappedCitation-14988249http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/14988249
http://purl.uniprot.org/uniprot/P09681http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/14988249
http://purl.uniprot.org/uniprot/P01275http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/14988249