Mostrar el registro sencillo del ítem
dc.contributor.author
Leiss, Veronika
dc.contributor.author
Flockerzie, Katarina
dc.contributor.author
Novakovic, Ana
dc.contributor.author
Rath, Michaela
dc.contributor.author
Schönsiegel, Annika
dc.contributor.author
Birnbaumer, Lutz
![Se ha confirmado la validez de este valor de autoridad por un usuario](/themes/CONICETDigital/images/authority_control/invisible.gif)
dc.contributor.author
Schürmann, Annette
dc.contributor.author
Harteneck, Christian
dc.contributor.author
Nürnberg, Bernd
dc.date.available
2020-03-06T13:22:20Z
dc.date.issued
2014-11-01
dc.identifier.citation
Leiss, Veronika; Flockerzie, Katarina; Novakovic, Ana; Rath, Michaela; Schönsiegel, Annika; et al.; Insulin secretion stimulated by L-arginine and its metabolite L-ornithine depends on Gα(i2); American Physiological Society; American Journal of Physiology - Endocrinology and Metabolism; 307; 1-11-2014; E800–E812
dc.identifier.issn
0193-1849
dc.identifier.uri
http://hdl.handle.net/11336/98903
dc.description.abstract
Bordetella pertussis toxin (PTx), also known as islet-activating protein, induces insulin secretion by ADP-ribosylation of inhibitory G proteins. PTx-induced insulin secretion may result either from inactivation of Gα(o) proteins or from combined inactivation of Gα(o), Gα(i1), Gα(i2), and Gα(i3) isoforms. However, the specific role of Gα(i2) in pancreatic β-cells still remains unknown. In global (Gα(i2)(-/-)) and β-cell-specific (Gα(i2)(βcko)) gene-targeted Gα(i2) mouse models, we studied glucose homeostasis and islet functions. Insulin secretion experiments and intracellular Ca²⁺ measurements were used to characterize Gα(i2) function in vitro. Gα(i2)(-/-) and Gα(i2)(βcko) mice showed an unexpected metabolic phenotype, i.e., significantly lower plasma insulin levels upon intraperitoneal glucose challenge in Gα(i2)(-/-) and Gα(i2)(βcko) mice, whereas plasma glucose concentrations were unchanged in Gα(i2)(-/-) but significantly increased in Gα(i2)(βcko) mice. These findings indicate a novel albeit unexpected role for Gα(i2) in the expression, turnover, and/or release of insulin from islets. Detection of insulin secretion in isolated islets did not show differences in response to high (16 mM) glucose concentrations between control and β-cell-specific Gα(i2)-deficient mice. In contrast, the two- to threefold increase in insulin secretion evoked by L-arginine or L-ornithine (in the presence of 16 mM glucose) was significantly reduced in islets lacking Gα(i2). In accord with a reduced level of insulin secretion, intracellular calcium concentrations induced by the agonistic amino acid L-arginine did not reach control levels in β-cells. The presented analysis of gene-targeted mice provides novel insights in the role of β-cell Gα(i2) showing that amino acid-induced insulin-release depends on Gα(i2).
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Physiological Society
![Se ha confirmado la validez de este valor de autoridad por un usuario](/themes/CONICETDigital/images/authority_control/invisible.gif)
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
PROTEINA G(i2)
dc.subject
INSULIN DOSING
dc.subject
GPCR
dc.subject.classification
Bioquímica y Biología Molecular
![Se ha confirmado la validez de este valor de autoridad por un usuario](/themes/CONICETDigital/images/authority_control/invisible.gif)
dc.subject.classification
Ciencias Biológicas
![Se ha confirmado la validez de este valor de autoridad por un usuario](/themes/CONICETDigital/images/authority_control/invisible.gif)
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
![Se ha confirmado la validez de este valor de autoridad por un usuario](/themes/CONICETDigital/images/authority_control/invisible.gif)
dc.title
Insulin secretion stimulated by L-arginine and its metabolite L-ornithine depends on Gα(i2)
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-10-28T18:26:49Z
dc.journal.volume
307
dc.journal.pagination
E800–E812
dc.journal.pais
Estados Unidos
![Se ha confirmado la validez de este valor de autoridad por un usuario](/themes/CONICETDigital/images/authority_control/invisible.gif)
dc.journal.ciudad
Bethesda
dc.description.fil
Fil: Leiss, Veronika. University of Tübingen. Department of Pharmacology and Experimental Therapy; Alemania
dc.description.fil
Fil: Flockerzie, Katarina. University of Tübingen. Department of Pharmacology and Experimental Therapy; Alemania
dc.description.fil
Fil: Novakovic, Ana. University of Tübingen. Department of Pharmacology and Experimental Therapy; Alemania
dc.description.fil
Fil: Rath, Michaela. German Institute of Human Nutrition. Department of Experimental Diabetology; Alemania
dc.description.fil
Fil: Schönsiegel, Annika. University of Tübingen. Department of Pharmacology and Experimental Therapy; Alemania
dc.description.fil
Fil: Birnbaumer, Lutz. National Institute ofEnvironmental Health Sciences. Laboratory of Neurobiology; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Schürmann, Annette. German Institute of Human Nutrition. Department of Experimental Diabetology; Alemania
dc.description.fil
Fil: Harteneck, Christian. University of Tübingen. Department of Pharmacology and Experimental Therapy; Alemania
dc.description.fil
Fil: Nürnberg, Bernd. University of Tübingen. Department of Pharmacology and Experimental Therapy; Alemania
dc.journal.title
American Journal of Physiology - Endocrinology and Metabolism
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://journals.physiology.org/doi/full/10.1152/ajpendo.00337.2014
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/ajpendo.00337.2014
Archivos asociados