R
Rüdiger Göke
Researcher at University of Marburg
Publications - 96
Citations - 7289
Rüdiger Göke is an academic researcher from University of Marburg. The author has contributed to research in topics: Receptor & Insulin. The author has an hindex of 39, co-authored 95 publications receiving 7056 citations. Previous affiliations of Rüdiger Göke include University of Göttingen & University of Michigan.
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Journal ArticleDOI
Exendin-4 is a high potency agonist and truncated exendin-(9-39)-amide an antagonist at the glucagon-like peptide 1-(7-36)-amide receptor of insulin-secreting beta-cells.
Rüdiger Göke,Hans-Christoph Fehmann,T. Linn,Harald Schmidt,Michael Krause,J. Eng,Burkhard Göke +6 more
TL;DR: Exendin-4 is an agonist and exendin-(9-39)-amide is a specific GLP-1 receptor antagonist, and both peptides stimulated the proinsulin gene expression at the level of transcription and reduced the effects of cAMP.
Journal ArticleDOI
Central administration of GLP-1-(7-36) amide inhibits food and water intake in rats
Mads Tang-Christensen,Philip J. Larsen,Rüdiger Göke,Anders Fink-Jensen,D. S. Jessop,M. Moller,S. P. Sheikh +6 more
TL;DR: In conclusion, GLP-1 may play a physiological role in regulation of both ingestion and the water and salt homeostasis and had no effect in behavioral assays measuring exploratory locomotor activity and conditioned taste aversion.
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Glucagon-like peptide-1 cells in the gastrointestinal tract and pancreas of rat, pig and man.
TL;DR: A highly specific monoclonal antibody directed against the C-terminal part of glucagon-like peptide-1 (GLP-1) was raised to immunohistochemically evaluate the distribution of GLP1 containing cells in the entire gastrointestinal tract including pancreas of rat, pig and man.
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Cell and molecular biology of the incretin hormones glucagon-like peptide-I and glucose-dependent insulin releasing polypeptide
TL;DR: The connection between the gastrointestinal tract and the endocrine pancreas was shown in the 1960s when insulin became measurable in plasma and the insulin response to oral glucose and intravenous glucose, resulting in neaemia, was shown.
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Glucagon-like peptide-1 and glucose-dependent insulin-releasing polypeptide plasma levels in response to nutrients
TL;DR: It is hypothesize that in contrast to GIP the GLP-1 release from L cells is triggered by nervous reflexes, by putative humoral factor(s) being released from the upper small intestine in addition to nutrient stimuli acting at the luminal surface of the gut.