Matches in UGent Biblio for { <https://biblio.ugent.be/publication/847351#aggregation> ?p ?o. }
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- aggregation classification "A1".
- aggregation creator B258027.
- aggregation creator B258028.
- aggregation creator B258029.
- aggregation creator B258030.
- aggregation creator B258031.
- aggregation creator B258032.
- aggregation creator B258033.
- aggregation creator B258034.
- aggregation creator person.
- aggregation date "1999".
- aggregation format "application/pdf".
- aggregation hasFormat 847351.bibtex.
- aggregation hasFormat 847351.csv.
- aggregation hasFormat 847351.dc.
- aggregation hasFormat 847351.didl.
- aggregation hasFormat 847351.doc.
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- aggregation hasFormat 847351.yaml.
- aggregation isPartOf urn:issn:0012-1797.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Altered cAMP and Ca2+ signaling in mouse pancreatic islets with glucagon-like peptide-1 receptor null phenotype".
- aggregation abstract "beta-Cells from rodents and humans express different receptors recognizing hormones of the secretin-glucagon family, which-when activated-synergize with glucose in the control of insulin release. We have recently reported that isolated islets from mice homozygous for a GLP-1 receptor null mutation (GLP-1R-/-) exhibit a well-preserved insulin-secretory response to glucose. This observation can be interpreted in two different ways: 1) the presence of GLP-1R is not essential for the secretory response of isolated islets to glucose alone; 2) beta-cells in GLP-1R-/- pancreases underwent compensatory changes in response to the null mutation. To explore these possibilities, we studied islets horn control GLP-1R+/+ mice in the absence or presence of 1 mu mol/l exendin (9-39)amide, a specific and potent GLP-1R antagonist. Exendin (9-39)amide (15-min exposure) reduced glucose-induced insulin secretion from both perifused and statically incubated GLP-1R+/+ islets by 50% (P < 0.05), and reduced islet cAMP production in parallel (P < 0.001), Furthermore, GLP-1R-/- islets exhibited: 1) reduced cAMP accumulation in the presence of 20 mmol/l glucose (knockout islets versus control islets, 12 +/- 1 vs. 27 +/- 3 fmol.islet(-1).15 min(-1) P < 0.001) and exaggerated acceleration of cAMP production by 10 nmol/l glucose-dependent insulinotropic peptide (GIP) (increase over 20 mmol/l glucose by GIP in knockout islets versus control islets: 66 +/- 5 vs, 14 +/- 3 fmol.islet(-1).15 min(-1) P < 0.001); 2) increased mean cytosolic [Ca2+] ([Ca2+](c)) at 7, 10, and 15 mmol/l glucose in knockout islets versus control islets; and 3) signs of asynchrony of [Ca2+], oscillations between different islet subregions. In conclusion, disruption of GLP-1R signaling is associated with reduced basal but enhanced GIP-stimulated cAMP production and abnormalities in basal and glucose-stimulated [Ca2+](c). These abnormalities suggest that GLP-1R signaling is an essential upstream component of multiple beta-cell signaling pathways.".
- aggregation authorList BK534380.
- aggregation endPage "1986".
- aggregation issue "10".
- aggregation startPage "1979".
- aggregation volume "48".
- aggregation aggregates 855899.
- aggregation isDescribedBy 847351.
- aggregation similarTo diabetes.48.10.1979.
- aggregation similarTo LU-847351.