Activation of Stat3 signaling in AgRP neurons promotes locomotor activity

Mesaros, A.; Koralov, S. B.; Rother, E.; Wunderlich, F. T.; Ernst, M. B.; Barsh, G. S.; Rajewsky, K.; Bruning, J. C.

doi:10.1016/j.cmet.2008.01.007

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Activation of Stat3 signaling in AgRP neurons promotes locomotor activity

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

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https://www.ncbi.nlm.nih.gov/pubmed/18316029
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Citation

Mesaros, A., Koralov, S. B., Rother, E., Wunderlich, F. T., Ernst, M. B., Barsh, G. S., et al. (2008). Activation of Stat3 signaling in AgRP neurons promotes locomotor activity. Cell Metab, 7(3), 236-48. doi:10.1016/j.cmet.2008.01.007.

Cite as: https://hdl.handle.net/21.11116/0000-000B-8067-0

Abstract

Leptin, an adipocyte-derived hormone, acts on hypothalamic neurons located in the arcuate nucleus (ARC) of the hypothalamus to regulate energy homeostasis. One of the leptin-regulated neuronal subtypes in the ARC are agouti-related peptide (AgRP)-expressing neurons, which are involved in the regulation of food intake and are directly inhibited by leptin. Leptin activates the signal transducer and activator of transcription 3 (Stat3), but the role of Stat3 in the regulation of AgRP neurons is unclear. Here we show that mice expressing a constitutively active version of Stat3 selectively in AgRP neurons are lean and exhibit relative resistance to diet-induced obesity. Surprisingly, this phenotype arises from increased locomotor activity in the presence of unaltered AgRP expression. These data demonstrate that Stat3-dependent signaling in AgRP neurons in the ARC controls locomotor activity independently of AgRP regulation.