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

Konner, A. C.; Hess, S.; Tovar, S.; Mesaros, A.; Sanchez-Lasheras, C.; Evers, N.; Verhagen, L. A.; Bronneke, H. S.; Kleinridders, A.; Hampel, B.; Kloppenburg, P.; Bruning, J. C.

doi:10.1016/j.cmet.2011.03.021

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

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

MPS-Authors

/persons/resource/persons129362

Mesaros, A.
Phenotyping, Core Facilities, Max Planck Institute for Biology of Ageing, Max Planck Society;

External Resource

https://www.ncbi.nlm.nih.gov/pubmed/21641553
(Any fulltext)

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

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.

Cite as: https://hdl.handle.net/21.11116/0000-000B-82BB-F

Abstract

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.