Showing papers by "Rüdiger Göke published in 1992"
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.
Abstract: 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 GLP-1 containing cells in the entire gastrointestinal tract including pancreas of rat, pig and man. In the pancreas GLP-1-immunoreactive cells were found variously shaped and predominantly located in the periphery of the islets. Ultrastructurally, GLP-1 was co-localized with glucagon in the alpha-granula of A-cells and was mainly restricted to the electrondense core. In the intestine open type cells reaching the lumen via a slender apical process were stained with the GLP-1 antibody. They occurred in all parts of the crypts but predominantly in the basal portion. The density of GLP-1 immunoreactive cells varied between species in a characteristic order: rat greater than pig greater than man. In pig and human gut a large number of cells occurred in the distal jejunum and ileum. A continuous increase of cell densities was found from the proximal to the distal colon resulting in highest numbers in the rectum. In rats the highest cell density occurred in the ileum. Again, a continuous increase of GLP-1-positive cell numbers was evident from the proximal to the distal portion of small and large bowel. GLP-1 was partly co-localized with PYY. The GLP-1 positive cells appeared electronmicroscopically as L-cells with the typical large granula. This morphological data indicates that GLP-1-releasing cells in the small intestine are appropriately positioned in the distal part to sense and respond to the presence of nutrients that have escaped the absorptive surface of the upper small intestine.
608 citations
TL;DR: Glucagon-like peptide-1 is the main product of the intestinal processing of proglucagon and it is involved at several levels in the regulation of insulin synthesis and secretion.
74 citations
TL;DR: Solubilization of the GLP‐1(7–36)amide receptor in a functional state and opens up the possibility for further molecular characterization of the receptor protein.
37 citations
TL;DR: A slight but not dose-dependent stimulation of insulin secretion by supramaximal GLP-1 loads under basal glucose levels was found, but the necessary GLp-1 concentrations to achieve this in vitro effect are beyond physiological or postprandial levels.
25 citations
TL;DR: Normal transcription and postranslational processing of the preprotachykinin (PPT)‐I gene and regulated release of substance P and neurokinin A by the rat pancreatic endocrine cell‐line, RINm5F, has been demonstrated, using radioimmunoassays, reversed‐phase (rp)HPLC and Northern blot analysis.
12 citations
TL;DR: R rab3a is expressed in rat insulin‐releasing insulinoma‐derived RIN‐cells with a specific 1800 bp transcription product.
10 citations
TL;DR: In this paper, an insulin-secreting subclone of a rat insulinoma cell line was incubated in serum-free medium up to 24 hours in the presence or absence of glucagon-like peptide-1(7-36)amide in various concentrations, 3-isobutyl-1 methylxanthine (1 mM), choleratoxin (10 nM), carbachol ( 1 mM), and potassium (40 mM).
Abstract: RINm5F cells, an insulin-secreting subclone of a rat insulinoma cell line, were incubated in serum-free medium up to 24 hours in the presence or absence of glucagonlike peptide-1(7-36)amide in various concentrations, 3-isobutyl-1 methylxanthine (1 mM), choleratoxin (10 nM), carbachol (1 mM), and potassium (40 mM). Insulin release and biosynthesis were measured by the immunoreactive insulin content of the cells and the medium. Steady-state levels of insulin-specific mRNA were determined by Northern and slot blot analysis. Short-term insulin release is significantly stimulated by all secretagogues tested. A significant increase of insulin biosynthesis by any of the various secretagogues was not detectable on the peptide and mRNA level. Sodium butyrate (1 mM), a differentiating agent, increased insulin-specific mRNA levels in RINm5F cells after 72 hours. In conclusion, substances known to stimulate short-term insulin release in RINm5F cells do not stimulate insulin biosynthesis, indicating an uncoupling of insulin secretion and biosynthesis in these transformed beta cells.
3 citations