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Zeitschriftenartikel

Role for insulin signaling in catecholaminergic neurons in control of energy homeostasis

MPG-Autoren

Konner,  A. C.
Max Planck Society;

Hess,  S.
Max Planck Society;

Tovar,  S.
Max Planck Society;

Mesaros,  A.
Max Planck Society;

Sanchez-Lasheras,  C.
Max Planck Society;

Evers,  N.
Max Planck Society;

Verhagen,  L. A.
Max Planck Society;

Bronneke,  H. S.
Max Planck Society;

Kleinridders,  A.
Max Planck Society;

Hampel,  B.
Max Planck Society;

Kloppenburg,  P.
Max Planck Society;

Bruning,  J. C.
Max Planck Society;

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Zitation

Konner, A. C., Hess, S., Tovar, S., Mesaros, A., Sanchez-Lasheras, C., Evers, N., et al. (2011). Role for insulin signaling in catecholaminergic neurons in control of energy homeostasis. Cell Metab, 13(6), 720-8. doi:10.1016/j.cmet.2011.03.021.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0028-5929-7
Zusammenfassung
Dopaminergic midbrain neurons integrate signals on food palatability and food-associated reward into the complex control of energy homeostasis. To define the role of insulin receptor (IR) signaling in this circuitry, we inactivated IR signaling in tyrosine hydroxylase (Th)-expressing cells of mice (IR(DeltaTh)). IR inactivation in Th-expressing cells of mice resulted in increased body weight, increased fat mass, and hyperphagia. While insulin acutely stimulated firing frequency in 50% of dopaminergic VTA/SN neurons, this response was abolished in IR(DeltaTh) mice. Moreover, these mice exhibited an altered response to cocaine under food-restricted conditions. Taken together, these data provide in vivo evidence for a critical role of insulin signaling in catecholaminergic neurons to control food intake and energy homeostasis.