Loss of Cytokine-STAT5 Signaling in the CNS and Pituitary Gland Alters Energy Balance and Leads to Obesity
Open accessAbstract
Signal transducers and activators of transcription (STATs) are critical components of cytokine signaling pathways. STAT5A and STAT5B (STAT5), the most promiscuous members of this family, are highly expressed in specific populations of hypothalamic neurons in regions known to mediate the actions of cytokines in the regulation of energy balance. To test the hypothesis that STAT5 signaling is essential to energy homeostasis, we used Cre-mediated recombination to delete the Stat5 locus in the CNS. Mutant males and females developed severe obesity with hyperphagia, impaired thermal regulation in response to cold, hyperleptinemia and insulin resistance. Furthermore, central administration of GM-CSF mediated the nuclear accumulation of STAT5 in hypothalamic neurons and reduced food intake in control but not in mutant mice. These results demonstrate that STAT5 mediates energy homeostasis in response to endogenous cytokines such as GM-CSF.
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Neuronal deletion of STAT5 in mice causes a mild-obesity phenotype.
“neuronal deletion of STAT5 in mice (via RIP-cre or Nestin-cre) causes a mild-obesity phenotype (101).”
From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [101]
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References 27 · Cited by 90
Research works printed but not linked: 2
- [26]Cui Y Riedlinger G Miyoshi K Tang W Li C 2004 Inactivation of Stat5 in mouse mammary epithelium during pregnancy reveals distinct functions in cell proliferation, survival, and differentiation. Mol Cell Biol 24 8037 8047 15340066 PMC515028
- [27]Tronche F Kellendonk C Kretz O Gass P Anlag K 1999 Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety. 23 99 103 10471508
- Authors
- Lee, J.-Y., Muenzberg, H., Gavrilova, O., Reed, J. A., Berryman, D., Villanueva, E. C., Louis, G. W., Leinninger, G. M., Bertuzzi, S., Seeley, R. J., Robinson, G. W., Myers, M. G., & Hennighausen, L.
- Affiliations
- National Institutes of Health (US)
- University of Michigan (US)
- University of Cincinnati (US)
- Ohio University (US)
- Corresponding author
- Hennighausen, Lothar
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2008-02-20
- Volume
- 3
- Issue
- 2
- Pages
- e1639
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC2237899
- OpenAlex
- W2095456538
- Cited by
- 90
- References
- 27
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 1 · 2021: 7 · 2020: 5 · 2019: 9 · 2018: 3 · 2017: 5 · 2016: 5 · 2015: 13 · 2014: 5 · 2013: 9 · 2012: 4
- FWCI
- 2.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, public-domain)
- PubMed Central (publishedVersion, public-domain)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Australian Government
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- STAT5, STAT5A, STAT5B, cytokine signaling, energy homeostasis, obesity, hypothalamic neurons, GM-CSF, hyperphagia, leptin, insulin resistance, thermoregulation, pituitary gland, central nervous system, conditional knockout mice
- MeSH terms
- Animals, Central Nervous System, Energy Metabolism, Female, Homeostasis, Hypothalamus, Male, Mice, Transgenic, Neurons, Obesity, Pituitary Gland, Signal Transduction, Cytokines, Active Transport, Cell Nucleus, STAT5 Transcription Factor, Mice
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