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  An Obesity-Predisposing Variant of the FTO Gene Regulates D2R-Dependent Reward Learning

Sevgi, M., Rigoux, L., Kuehn, A. B., Mauer, J., Schilbach, L., Hess, M. E., et al. (2015). An Obesity-Predisposing Variant of the FTO Gene Regulates D2R-Dependent Reward Learning. JOURNAL OF NEUROSCIENCE, 35(36), 12584-12592. doi:10.1523/JNEUROSCI.1589-15.2015.

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Sevgi, Meltem1, Autor
Rigoux, Lionel1, Autor
Kuehn, Anne B.1, Autor
Mauer, Jan1, Autor
Schilbach, Leonhard2, Autor           
Hess, Martin E.1, Autor
Gruendler, Theo O. J.1, Autor
Ullsperger, Markus1, Autor
Stephan, Klaas Enno1, Autor
Bruening, Jens C.1, Autor
Tittgemeyer, Marc1, Autor
Affiliations:
1external, ou_persistent22              
2Max Planck Institute of Psychiatry, Max Planck Society, ou_1607137              

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Schlagwörter: dopamine, fMRI, genetics, modeling, obesity; reinforcement learning
 Zusammenfassung: Variations in the fat mass and obesity-associated (FTO) gene are linked to obesity. However, the underlying neurobiological mechanisms by which these genetic variants influence obesity, behavior, and brain are unknown. Given that Fto regulates D2/3R signaling in mice, we tested in humans whether variants in FTO would interact with a variant in the ANKK1 gene, which alters D2R signaling and is also associated with obesity. In a behavioral and fMRI study, we demonstrate that gene variants of FTO affect dopamine (D2)-dependent midbrain brain responses to reward learning and behavioral responses associated with learning from negative outcome in humans. Furthermore, dynamic causal modeling confirmed that FTO variants modulate the connectivity in a basic reward circuit of meso-striato-prefrontal regions, suggesting a mechanism by which genetic predisposition alters reward processing not only in obesity, but also in other disorders with altered D2R-dependent impulse control, such as addiction.

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Sprache(n): eng - English
 Datum: 2015-09-09
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: ISI: 000363659300023
DOI: 10.1523/JNEUROSCI.1589-15.2015
 Art des Abschluß: -

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Titel: JOURNAL OF NEUROSCIENCE
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: Washington DC 2005 : Society for Neuroscience
Seiten: - Band / Heft: 35 (36) Artikelnummer: - Start- / Endseite: 12584 - 12592 Identifikator: ISSN: 0270-6474