6 results on '"Stadlbauer, Karin"'
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2. Evidence that the multiflorine‐derived substituted quinazolidine 55P0251 augments insulin secretion and lowers blood glucose via antagonism at α2‐adrenoceptors in mice.
- Author
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Lehner, Zsuzsanna, Stadlbauer, Karin, Brunmair, Barbara, Adorjan, Immanuel, Genov, Miroslav, Kautzky‐Willer, Alexandra, Scherer, Thomas, Scheinin, Mika, Bauer, Leonhardt, and Fürnsinn, Clemens
- Subjects
- *
BLOOD sugar , *OXYGEN in the blood , *BINDING site assay , *GLUCOSE tolerance tests , *SECRETION - Abstract
Aims: To investigate the mechanism of action of 55P0251, a novel multiflorine‐derived substituted quinazolidine that augments insulin release and lowers blood glucose in rodents, but does not act via mechanisms addressed by any antidiabetic agent in clinical use. Materials and Methods: Using male mice, we determined the effects of 55P0251 on glucose tolerance, insulin secretion from isolated islets and blood oxygen saturation, including head‐to‐head comparison of 55P0251 to its inverted enantiomer 55P0250, as well as to other anti‐hyperglycaemic multiflorine derivatives discovered in our programme. Results: 55P0251 was clearly superior to its inverted enantiomer in the glucose tolerance test (area under the curve: 11.3 mg/kg 55P0251, 1.19 ± 0.04 min*mol/L vs 55P0250, 1.80 ± 0.04 min*mol/L; P <.0001). For insulin release in vitro, this superiority became visible only under concomitant adrenergic background stimulation (glucose‐stimulated insulin release, fmol*islet−1*30 min−1: without α2‐adrenoceptor agonist: 500 μmol/L 55P0251, 390 ± 34, vs 55P0250, 459 ± 40, nonsignificant; with α2‐adrenoceptor agonist: 250 μmol/L 55P0251, 138 ± 9, vs 55P0250, 21 ± 6; P <.0001). Since receptor binding assays suggested antagonism at α2A‐adrenoceptors as a potential mechanism of action, we measured oxygen saturation in capillary blood from the tail as a surrogate of vasoconstriction, which supported α2‐antagonistic action in vivo (90 mg/kg 55P0251, 83 ± 3%, vs 55P0250, 57 ± 3%; P <.0001). Lack of association between glucose‐lowering activities and α2A‐adrenoceptor binding affinity arising from comparison of multiflorine derivatives was attributed to differences in their pharmacokinetic properties. Conclusions: Our findings suggest that 55P0251 and related multiflorine derivatives are to be categorized as α2‐adrenoceptor antagonists with potential to lower blood glucose by blocking α2A‐adrenoceptors on pancreatic β cells. [ABSTRACT FROM AUTHOR]
- Published
- 2020
- Full Text
- View/download PDF
3. Preclinical characterization of 55P0251, a novel compound that amplifies glucose-stimulated insulin secretion and counteracts hyperglycaemia in rodents
- Author
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Stadlbauer, Karin, primary, Brunmair, Barbara, additional, Lehner, Zsuzsanna, additional, Adorjan, Immanuel, additional, Scherer, Thomas, additional, Luger, Anton, additional, Bauer, Leonhardt, additional, and Fürnsinn, Clemens, additional
- Published
- 2017
- Full Text
- View/download PDF
4. Hirngespinste. Über neuronale Wahrheiten psychischer Erkrankungen
- Author
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Stadlbauer, Karin
- Abstract
Im Rahmen dieses Diplomprojekts steht der gegenwärtig vorherrschende, biologisch-neurowissenschaftliche Diskurs rund um die Erklärungen psychischer Erkrankungen im Fokus. Nach einer Auseinandersetzung mit biologischem Wissen im Feld der Psychologie im Allgemeinen und in dem der Klinischen Psychologie und Psychiatrie im Besonderen, folgt eine Beschäftigung mit diskurstheoretischen Ansätzen und den Überlegungen Foucaults zur Verbindung von Wissen und Macht. Vor diesem Hintergrund wird folgende Forschungsfrage leitend: Welche diskursiven Strategien der Neurowissenschaften in Bezug auf psychische Erkrankungen lassen sich aus dem vorliegenden Material rekonstruieren? Wie werden psychische Erkrankungen in biologisch-neurowissenschaftlichen Texten dargestellt? Wie wird dabei ‚Wahrheit‘ produziert und Glaubwürdigkeit hergestellt? Zur Beantwortung der Fragestellung werden, an der Fakultät für Psychologie an der Universität Wien prüfungsrelevante, in erster Linie biologische Lehrbuchinhalte, im Rahmen derer psychische Erkrankungen behandelt werden, einer kritisch-diskursanalytischen Untersuchung unterzogen. Die Ergebnisse der Analyse zeigen, dass der Vollzug des biologisch-neurowissenschaftlichen Narrativs abstrahiert und weit entfernt von Phänomenen des subjektiven Erlebens in einer Welt isolierter und biologisch anormalisierter Gehirne stattfindet. Daraus ergibt sich nicht nur eine Distanzierung von einem Erlebten und Gelebten, sondern auch eine De-Kontextualisierung und Individualisierung umfassender, weitläufiger Phänomene in die Sphäre der Biologie des einzelnen Individuums. Dies entfaltet sich in einem, als naturwissenschaftlich-biologisch gerahmten Expertendiskurs, wobei dem diskursiven Einsatz von Hirnbildlichkeiten eine entscheidende, ‚wahrheitsverleihende‘ Funktion zukommt. Der untersuchte Diskurs wird als einziger als Diskurs der ‚Wahrheit‘ zugelassen, während alternative Diskurse inkorporiert oder überhaupt ausgelassen werden. An der Untersuchung des biologisch-neurowissenschaftlichen Diskurses über psychische Erkrankungen soll beispielhaft die zentrale Rolle von biologischen Wissensformationen im Macht-Wissen-Komplex im Feld der Psychologie aufgezeigt werden., Within the framework of this thesis, the focus lies on the current biological-scientific discourse on mental illness. After a basic discussion of biological knowledge in the field of psychology in general and in that of clinical psychology in particular, follows a debate of discourse analytic approaches and the considerations of Foucault regarding the connection of knowledge and power. The empirical investigation is guided by the following questions: Which discursive strategies of the Neurosciences regarding mental illness can be reconstructed? How is mental illness constructed? What are the rules of knowledge-production and how is credibility reached? To give answers to the research questions, contents of textbooks that deal with mental illness from a biological view and that are used for teaching at the Faculty of Psychology at the University of Vienna are examined through the method of critical discourse analysis. The results found within this investigation show that the performance of the biological neuroscientific discourse takes place in an abstracted and distant world of isolated and biological anormalized brains. Besides being an alienation from experienced and actually lived phenomenons, it also results in the decontextualization and individualisation of complex and vast phenomenons in the biological sphere of an individual. This is reached by developing a scientific-biological framed expert discourse, in which the discoursive use of brain scans is seen to have a decisive weight. The examined discourse seems to become the only valid discourse of ‚truth‘, while alternative discourses get incorporated or left out. This thesis and its containing analysis of the biological neuroscientific discourse on mental illness serves as an example that highlights the crucial role of knowledge used in the field of Psychology in the knowledge-power-complex.
- Published
- 2015
- Full Text
- View/download PDF
5. 55P0110, a Novel Synthetic Compound Developed from a Plant Derived Backbone Structure, Shows Promising Anti-Hyperglycaemic Activity in Mice
- Author
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Brunmair, Barbara, primary, Lehner, Zsuzsanna, additional, Stadlbauer, Karin, additional, Adorjan, Immanuel, additional, Frobel, Klaus, additional, Scherer, Thomas, additional, Luger, Anton, additional, Bauer, Leonhardt, additional, and Fürnsinn, Clemens, additional
- Published
- 2015
- Full Text
- View/download PDF
6. Evidence that the multiflorine-derived substituted quinazolidine 55P0251 augments insulin secretion and lowers blood glucose via antagonism at α 2 -adrenoceptors in mice.
- Author
-
Lehner Z, Stadlbauer K, Brunmair B, Adorjan I, Genov M, Kautzky-Willer A, Scherer T, Scheinin M, Bauer L, and Fürnsinn C
- Subjects
- Alkaloids, Animals, Insulin Secretion, Male, Mice, Receptors, Adrenergic, alpha-2 metabolism, Blood Glucose, Insulin metabolism
- Abstract
Aims: To investigate the mechanism of action of 55P0251, a novel multiflorine-derived substituted quinazolidine that augments insulin release and lowers blood glucose in rodents, but does not act via mechanisms addressed by any antidiabetic agent in clinical use., Materials and Methods: Using male mice, we determined the effects of 55P0251 on glucose tolerance, insulin secretion from isolated islets and blood oxygen saturation, including head-to-head comparison of 55P0251 to its inverted enantiomer 55P0250, as well as to other anti-hyperglycaemic multiflorine derivatives discovered in our programme., Results: 55P0251 was clearly superior to its inverted enantiomer in the glucose tolerance test (area under the curve: 11.3 mg/kg 55P0251, 1.19 ± 0.04 min*mol/L vs 55P0250, 1.80 ± 0.04 min*mol/L; P < .0001). For insulin release in vitro, this superiority became visible only under concomitant adrenergic background stimulation (glucose-stimulated insulin release, fmol*islet
-1 *30 min-1 : without α2 -adrenoceptor agonist: 500 μmol/L 55P0251, 390 ± 34, vs 55P0250, 459 ± 40, nonsignificant; with α2 -adrenoceptor agonist: 250 μmol/L 55P0251, 138 ± 9, vs 55P0250, 21 ± 6; P < .0001). Since receptor binding assays suggested antagonism at α2A -adrenoceptors as a potential mechanism of action, we measured oxygen saturation in capillary blood from the tail as a surrogate of vasoconstriction, which supported α2 -antagonistic action in vivo (90 mg/kg 55P0251, 83 ± 3%, vs 55P0250, 57 ± 3%; P < .0001). Lack of association between glucose-lowering activities and α2A -adrenoceptor binding affinity arising from comparison of multiflorine derivatives was attributed to differences in their pharmacokinetic properties., Conclusions: Our findings suggest that 55P0251 and related multiflorine derivatives are to be categorized as α2 -adrenoceptor antagonists with potential to lower blood glucose by blocking α2A -adrenoceptors on pancreatic β cells., (© 2019 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd.)- Published
- 2020
- Full Text
- View/download PDF
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